Can the human body survive in a zero sugar diet strictly through gluconeogenesis?

Can the human body survive in a zero sugar diet strictly through gluconeogenesis?

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I read an article a while back about athletes (I believe cyclists) being exposed to a 0 sugar diet and their blood sugar levels stayed relatively constant, which prompted the question whether people could survive strictly off a no sugar diet.

How You Can Have High Blood Sugar Without Carbs

Can you have high blood sugar without carbs? Well, it’s important to look at common beliefs about high blood sugar first.

High blood sugar is bad. Carbohydrates raise blood sugar. Therefore carbohydrates are bad.” The theory is simple, and yet incredibly flawed.

The truth is, you can have chronically high blood sugar even while religiously avoiding every starch and sugar in sight. Low-carb forums are littered with posts asking a very relevant question:

Why is my blood sugar so high when I’m not eating any carbs?

The answer is simple, yet often overlooked.

Figure 3) The Actions of the Three Enzymes

How Acetaldehyde Dehydrogenase Works

There are several varieties of aldehyde dehydrogenase found in the human body. The one which normally breaks down acetaldehyde is called ALDH2. There is another variety aldehyde dehydrogenase found in the human body which is called ALDH2*2. ALDH2*2 is only about 8% as efficient as ALDH2 in metabolizing acetaldehyde. Some East Asian people have ALDH2*2 instead of ALDH2 in their bodies. These individuals find the effect of alcohol to be very unpleasant as we discuss below.

The aldehyde dehydrogenase enzymes are found in many tissues of the body, but are at the highest concentration in the liver

The Problem with Too Much NADH

Alcohol Affects Some People Differently from Others

East Asians and American Indians: Most individuals use a form of acetaldehyde dehydrogenase called ALD2 to metabolize the acetaldehyde which results from alcohol metabolism. However, many East Asians and American Indians produce a form of acetaldehyde dehydrogenase called ALD2*2 which is far less efficient at breaking down acetaldehyde than ALD2. ALD2*2 is only about 8% as efficient as ALD2 at metabolizing acetaldehyde.

Additionally many East Asians and American Indians have a form of alcohol dehydrogenase that is more efficient at turning alcohol into acetaldehyde than that of people from other genetic backgrounds. The end result is that these people wind up with large amounts of the poisonous compound acetaldehyde in their bodies whenever they drink alcohol. This acetaldehyde causes their faces to flush and leads to headaches, nausea, vomiting, heart palpitations and other extreme physical unpleasantness. This reaction to alcohol is sometimes referred to as the "flush syndrome". The symptoms of flush syndrome are exactly the same as the symptoms caused in people who take the anti-drinking medication antabuse. Antabuse also causes a build-up of acetaldehyde within the body. As many as 50% of people of Japanese descent are estimated to show flush syndrome. Flush syndrome is more severe in some individuals than others. It is estimated that individuals with severe flush syndrome do not develop alcohol problems because they find drinking alcohol to be extremely unpleasant.

Older Males: As men age they tend to produce less alcohol dehydrogenase. Older men are likely to become more intoxicated on smaller amounts of alcohol than younger men. Alcohol dehydrogenase in women is apparently not affected by age.

Menopausal Women: Apparently hormone changes which occur at menopause can cause menopausal women to become more intoxicated on smaller doses of alcohol.

People with Liver Damage: People with liver damage produce less alcohol dehydrogenase than do those with healthy livers and thus can become more intoxicated on smaller doses of alcohol. This phenomenon is referred to as Reverse Tolerance.

Frequent Heavy Drinkers: Frequent heavy drinkers produce more alcohol dehydrogenase than other people and thus become less intoxicated on larger quantities of alcohol. These people can metabolize up to 38 ml (over 2 standard drinks) of alcohol per hour whereas the average person metabolizes only around 13 ml (about 0.7 standard drinks) per hour.

How Antabuse Works

Why You Shouldn't Drink on an Empty Stomach

What You Drink Does Matter!!

Alcohol Concentration: Many people find that they get much more intoxicated when drinking straight vodka than they do when drinking beer. This is because they get a lot more alcohol in their bodies in a lot shorter period of time when drinking the vodka. As a general rule of thumb the less concentrated the alcohol in a drink the less alcohol one will put into their body per hour.

Flavor: People also tend to drink strongly flavored drinks more slowly than tasteless drinks. So most people will get more alcohol into their system per hour when drinking vodka than they will when drinking whiskey.

Carbonation: Carbonation speeds the absorption of alcohol into the bloodstream. People drinking carbonated drinks will become intoxicated more quickly and achieve higher BACs than people dinking the same amount of alcohol per hour in the form of non-carbonated drinks. There is, however, a trade-off here because many people drink carbonated drinks more slowly than non-carbonated drinks.

Diet Soda: Diet soda interacts with alcohol too, so people who drink mixed drinks made with diet soda will become intoxicated more quickly and achieve higher BACS than people drinking identical drinks made with regular soda. Researchers in Adelaide, Australia found that the stomach emptied into the small intestine in 21.1 minutes for the people who drank mixed drinks made with diet soda. When people drank drinks made with regular soda, the stomach emptied in 36.3 minutes (P < .01). Peak blood alcohol concentration was 0.053 g% for the diet drinks and 0.034 g% with the regular drinks.

Beware Mixing Alcohol with Your Medications

You should check this reference if you have any concerns about the interaction of a medication which you are taking with alcohol. Just for a quick reference we will note here some very common Over The Counter (OTC) and prescriptions medications and a few other substances which you should be very cautious about mixing with alcohol. Some of them may surprise you.

Aspirin: For some reason we are not quite sure of aspirin appears to block the action of alcohol dehydrogenase. What this means is that if you take aspirin before drinking you will became much more intoxicated on a much smaller dose of alcohol than usual. It is generally recommended that you do not take aspirin for around six hours before drinking alcohol. If you have taken aspirin before drinking be cautious and try to limit your alcohol intake as much as possible.

Cayenne pepper: Cayenne pepper dilates the blood vessels and apparently leads higher BACs and more exposure of the brain to alcohol. In short if you drink alcohol while ingesting a lot of cayenne pepper you will become much drunker than usual. Avoid red pepper vodka!

Tylenol (acetaminophen, paracetamol): Even by itself Tylenol can cause liver failure. Combining Tylenol with alcohol is a horrible one two punch to the liver. If you love your liver then don't take Tylenol or Tylenol PM or anything else containing acetaminophen with alcohol or when you are hungover. Else you might as well fry up your liver with onions!!

Ambien: mixing alcohol with ambien is just about a sure recipe for a blackout or a brownout. People who mix the two also often report sleepwalking or even sleep eating. Best to take one or the other and not mix them together.

Narcotic painkillers: Another recipe for blackout and disturbed behavior. Avoid mixing alcohol with Percocet, percodan, vicodin, oxycontin, codeine, morphine or any other narcotic pain killers.

Benadryl (diphenhydramine), Dramamine (dimenhydrinate), and Unisom Nighttime (doxylamine): Mixing alcohol with any antihistamine which causes drowsiness will definitely enhance the feeling of drowsiness many times over. All OTC sleep aids consist of one of the three above named antihistamines. Mixing them with alcohol is not medically dangerous, but beware of the added drowsiness.

The Effect of Smoking Tobacco (Nicotine):

Routes of Alcohol Ingestion

Inhalation: AWOL (Alcohol With Out Liquid) is an alcohol inhalation device that has been released in the US and the UK. AWOL's manufacturers claim that when alcohol is vaporized and inhaled it can lead to intoxication as much as 10 times as quickly as drinking and allows one to sober up with no hangover in an equally rapid time frame. Doctors are still debating the safety of AWOL. At least 22 states in the US have banned AWOL.

Injection: Some scientific researchers give alcohol injections to research subjects when they wish to bypass the stomach. It was the comparison of the effects of injected alcohol with orally ingested alcohol which led scientists to conclude that women have less alcohol dehydrogenase in their stomachs than men do. Self-administration of alcohol by injection is extremely dangerous and should never be attempted. The risk of death by alcohol poisoning is extremely high.

Alcohol enema: This is another rather dangerous and sometimes deadly form of alcohol administration. If the internet is to be believed then alcohol enemas are not uncommon at sex parties. A beer enema might be safe enough. However the simple fact is that alcohol is absorbed very rapidly through the large intestine and the rectum and there are no enzymes here to break it down. Thus the same dose of alcohol given by enema will produce a much higher BAC than if one drinks it. There was a famous case of death by sherry enema in Texas where the wife was acquitted of murder charges. And a vodka enema is silent but deadly for sure.

Transdermal: Alcohol can also be absorbed through the skin although this is quite a slow and impractical method of ingesting it.

Why Alcohol Has a Steady State Metabolism Rather Than a Half Life

Alcohol, on the other hand, shows a steady state metabolism not an exponential metabolism. The body of the average human metabolizes around 13 ml of alcohol per hour regardless. When we plot the metabolism of alcohol on a graph we get a straight line--in other words the rate of decay of alcohol is linear. Chemists refer to this as a Zero Order Reaction. The reason why alcohol has a steady state metabolism rather than a half-life metabolism is because the primary decay product of alcohol metabolism--acetaldehyde--is poisonous. The body must eliminate the acetaldehyde produced by the breakdown of alcohol before any more alcohol can be processed in order to avoid acetaldehyde poisoning. This slows down the rate of alcohol metabolism to a Zero Order Reaction rather than a First Order Reaction.

Figure 4 graphically illustrates the difference between steady state metabolism and half life metabolism.

Why Do Humans Have a Way To Break Down Alcohol?

Not only are we constantly ingesting alcohol along with the food we eat, our own bodies produce alcohol as a part of the digestive process. Our digestive tracts contain millions of micro-organisms which are necessary for us to properly digest our food. Among these micro-organisms are yeasts which produce alcohol from sugars within our own bodies.

With alcohol so omnipresent in nature it is necessary that animals have a way to break alcohol down, otherwise it would just accumulate in the body and no animal could function properly because the animals would always be constantly intoxicated.

Other alcohols such as methyl alcohol (wood alcohol) and isopropyl alcohol (rubbing alcohol) do not normally occur in nature. This is why we do not have a mechanism to break them down and why they are poisonous.

Poisonous Alcohols

Another highly poisonous alcohol is ethylene glycol (C2H6O2) which is used in antifreeze. A metabolite of ethylene glycol is the highly poisonous oxalic acid.

Rubbing alcohol (C3H8O)--also known as isopropyl alcohol--is more poisonous than ethanol but not as poisonous as methanol. Some chronic alcoholics turn to drinking rubbing alcohol when ethanol is unavailable--and some even come to prefer it.

Alcohol and Blood Sugar

Because of alcohol's effect on blood sugar people with diabetes are recommended to have no more than one or two standard drinks per day and to avoid drinks high in carbs. Untreated diabetes can lead to severe consequences including blindness, amputation of limbs affected by gangrene and even death--so diabetics are recommended to be especially cautious about their alcohol intake.


Frezza M, di Padova C, Pozzato G, Terpin M, Baraona E, Lieber CS. (1990). High blood alcohol levels in women. The role of decreased gastric alcohol dehydrogenase activity and first-pass metabolism. New England Journal of Medicine. Jan 11322(2):95-9.

Johnson RD, Horowitz M, Maddox AF, Wishart JM, Shearman DJ. (1991). Cigarette smoking and rate of gastric emptying: effect on alcohol absorption. BMJ. Jan 5302(6767):20-3.

MSNBC (2007). Elephants electrocuted in drunken rampage

Reuters. Charges dismissed in Texas sherry enema death - By Erwin Seba

Wu KL, Chaikomin R, Doran S, Jones KL, Horowitz M, Rayner CK. (2006). Artificially sweetened versus regular mixers increase gastric emptying and alcohol absorption. The American Journal of Medicine. Sep119(9):802-4.

AWOL - Alcohol Without liquid

Blood alcohol concentration. The Psychology Wiki.

Alcohol, Chemistry and You

Metabolism of Ethyl Alcohol in the Body

January 2001 Molecule of the Month

From Wikipedia, the free encyclopedia

From Wikipedia, the free encyclopedia

From Wikipedia, the free encyclopedia

Alcohol Metabolism Effects - Elmhurst College

Overview: How Is Alcohol Metabolized by the Body?

Role of Acetaldehyde in Mediating the Pharmacological and Behavioral Effects of Alcohol

UpToDate. Patient information: Diabetes mellitus type 2: Alcohol, exercise, and medical care

Read more about the Food Insulin index


19 thoughts on &ldquoWhat is the difference between glycemic index, the insulin index and insulin load?&rdquo

Reblogged this on Simple Living Over 50 and commented:
As time goes by I find more and more the truth being told about Type II Diabetes. Finally!

I have learned much from Dr. Fung’s videos. I’m glad I found them through this blog.

However, there has always been one thing that bothered me about these types of articles. “If you must eat, don’t eat carbs”. This is kind of like telling people not to put gas in their car. Carbs are the energy source for everything we do. Carbs and fat. You have to have some level of carbs in your system. Unless my understanding of biology is incorrect, if you were to go on a zero carb diet and stay on it permanently, you would eventually die.

So it would be helpful if these people made clear that “don’t eat carbs” is not a program you can follow forever. Carbs are a natural part of the food chain. It is simply that we eat them to excess, as we do so many other things, that is the problem. Unless I am completely mistaken.

I know, trust and respect a biologist who worked on the human genome project. I’m going to drop him a line and ask him that question specifically. I’ll follow up when I hear back from him.

I suggest you read “The World Turned Upside Down” to get the full context.

In the first chapter he says he said this as a joke at a conference, but then goes on to elaborate on the virtues of fasting, low carb and carbs that don’t raise your blood sugar.

In the end you need glucose, but as Rosedale will tell you, you can get that glucose via gluconeogenesis from protein.

I think you need to consider the total glucose load of your diet, not just carbs. That is, what proportion of the diet could convert to glucose in the system and require insulin.

I’m intrigued by the idea that there must be a ‘goldilocks’ zone of carbs plus protein that will provide adequate energy without excess insulin that would lead to fat loss.

The glycemic stuff is baloney. It was created using NON-DIABETICS and while I agree with the dangers of extra insulin, excess insulin is a response to excess glucose which comes from excess carbs and to a lesser degree excess protein. Treat the disease not the symptoms. control your carb and protein intake and you’ll have less glucose and less insulin response to deal with.

Diabetic t2 a1c 5.2
Meds free for 2 yrs

Not if you have reactive hypoglycemia (non-diabetic) like me. My insulin overreacts and is
different to “normal” and diabetics. Still trying to work out how to manage it. Clearly eating massive amounts of carbs aka DAA or diabetes australia recommends is just asking for constant hypos all day long, but even low carb I still deal with blood sugars below 4 for most of the day. Its quite frustrating trying to find the correct way to eat to avoid hypos and even harder to work out how to correct a hypo and not trigger another hypo 90 mins later. I hope with time, research and trial and error I work it out.

“You have to have some level of carbs in your system” – but you don’t have to eat them. The US IoM and others agree “The minimum level of dietary carbohydrates compatible with life is apparently zero”. Can you name a disease of carbohydrate deficiency ?

As a French scientist discovered, a dog eats no sugar but you can find sugar in the body of a dog – your liver will maintain blood glucose levels.

So I said I’d ask my biologist friend and post what he had to say. This was his answer:

To answer your Q, Yes, years ago, before all the nuances and alternate pathways of human metabolism were so fully understood it was believed that carbohydrates in some form (fats, sugars, starches…)were necessary to fuel the Citric Acid Cycle (CAC) in mitochondria to generate energy for the whole body (in the form of ATP) and glucose for use by the brain. The carbs could come either from your diet or your own body. But it is now known that in the absence of carbs the body can catabolize amino acids from proteins in your food and use the products as fuel. Specifically, under these low carb conditions the liver produces what are known as ketone bodies which cannot be metabolized by the liver itself but instead travel in the blood to the brain where they are used as an efficient fuel to power the CAC. There can be problems with overproduction of these ketone bodies if your diabetes is not well controlled, but if you’ve got a handle on that then there is no real physiological NEED for carbs. And apparently studies have shown that, at least for a matter of months, your body does not begin to cannibalize its own muscle mass -people actually lose a lot of their fat weight and PUT ON muscle. Sounds good to me.

However, even if you’re really trying, I think it would be really difficult to exclude ALL carbs from your diet. I mean, you gotta have some bacon, right?

Just got a revision, so I’m posting it here for clarity.

Yikes. On re-reading what I shot off to you yesterday I realize in my haste I threw fats in with carbs. This is of course an absurd mistake. Fats are broken down into fatty acids, eventually to acetyl CoA, which can be used for energy in the CAC -by all cells except neurons.

Yes. The body can survive (happily?) without carbs for a long time. Some interesting studies by Cahill are detailed in this –

I’m not sure starvation ketosis is optimal for the long term, however reducing your total glucose load to a point where you’re not storing fat and your blood sugars are well controlled makes a lot of sense to me!

The issue I have been having so far is that if I skip a meal or two my blood sugar immediately plummets to unsafe levels and I start experiencing the symptoms of hypoglycemia. So I am not sure how best to reduce my carbs without passing out at work or something.

Are you a type 1 or type 2? Sounds like you’re on insulin.

You’ll probably have to wind back your medications as you ease into the LCHF or IF approach while carefully monitoring your blood sugars.

What is the alkaline diet?

The alkaline diet is based on the theory that low body pH (acidity) can be harmful to one’s health, while high pH (alkalinity) is protective. In chemistry, pH is expressed using a 14-point scale, with zero being totally acidic and 14 being totally alkaline.

Proponents contend that the foods you eat can alter the pH level of blood—and therefore influence every system in the body. The theory is that when the body breaks down food to create energy, it leaves behind a residue known as ash. Ash can be acidic or alkaline, depending on what you’ve eaten.

According to alkaline theory, eating an acid-forming diet puts the body into a state of inflammation known as low-grade chronic metabolic acidosis. In addition, the theory continues, systemic stress arises from the body’s constant effort to neutralize pH levels. As a result, appetite-controlling hormones are disrupted, and cells receive a diminished supply of oxygen and nutrients, leaving the body susceptible to disease and weight gain.

On the flip side, according to believers, “alkalizing” foods do not form acidic ash. This supposedly eases strain on your system and keeps inflammation at bay. The diet’s fans say this can result in more energy, easier weight loss, and reduced risk of disease.

Classification of Biosurfactant Compounds From Bacteria Associated With Human Health

The antimicrobial BSs derived from microorganisms associated with human health can be categorized into two main classes: cell-associated and cell-released BSs (Supplementary Table 1).

Literature survey illustrates that the bacteria producing antimicrobial BSs associated with human health mostly belong to the phyla Firmicutes and Proteobacteria. Currently, the bacteria genera grouped within cell-associated BS class fall in the genera Lactobacillus and Pediococcus, while the cell-released BS class includes few strains of Lactobacillus, Pseudomonas, Bacillus, and Enterobacter genera (Figure 3).

Figure 3. Schematic representation of biosurfactants with antimicrobial activity produced by microorganisms associated with human health according to the human body districts. Bacteria enclosed in an orange box produce biosurfactants (BSs) with antimicrobial activity belonging to the cell-bound class bacteria enclosed in a light blue box produce BSs with antimicrobial activity released in the surrounding environment bacteria enclosed in an orange-light blue box produce BSs with antimicrobial activity belonging to both classes.

Cell-Associated Biosurfactants

The antimicrobial BSs from the Lactobacillus genus are generally cell-associated, probably for their intrinsic characteristics. The chemical analysis of characterized cell-associated BSs shows that they are high-molecular-weight molecules composed mainly of proteins, fatty acids, and sugars with different percentages.

Satpute et al. (2019) isolated a glycolipoprotein-type BS from Lactobacillus acidophilus NCIM 2903 with the ability to reduce the ST of 45 mN m 𠄱 (from 71 to 26 mN m 𠄱 ) and a critical micelle concentration (CMC) equal to 23.6 mg ml 𠄱 . The antibacterial and antiadhesive properties of the glycolipoprotein were detected at a concentration of 25 mg ml 𠄱 that was able to inhibit Escherichia coli NCIM 2065 and Proteus vulgaris NCIM 2027 growth of more than 30% and Bacillus subtilis MTCC 2423 growth of 26%. The action was not so potent against Pseudomonas putida MTCC 2467 (14% of growth inhibition). The stronger antiadhesive effect was against two Gram-positive bacteria as shown by 81% and 79% of inhibition of Staphylococcus aureus NCIM 2079 and B. subtilis MTCC 2423, respectively. Moreover, the cell-associated glycolipoprotein showed antiadhesive and antibiofilm potential against P. vulgaris NCIM 2027 and S. aureus NCIM 2079.

Similarly, antimicrobial BSs from Lactobacillus jensenii P6A and Lactobacillus gasseri P65 isolated from vaginal fluids of healthy women after 72 h of fermentation yield of 0.27 and 0.42 g L 𠄱 , respectively (Morais et al., 2017). The BSs produced by L. jensenii P6A and L. gasseri P65 reduced the water-surface tension of 28.8 mN m 𠄱 (from 72 to 43.2 mN m 𠄱 ) and 29.5 mN m 𠄱 (from 72 to 42.5 mN m 𠄱 ) with comparable CMC values of 7.1 and 8.58 mg ml 𠄱 , respectively. They also shared a similar chemical composition: P6A molecule was composed of 51.49% of carbohydrates, 15.17% of proteins, and 29.45% of lipids, while P65 was composed of 38.61% of carbohydrates, 9.81% of proteins, and 49.53% of lipids. Considering the last constituent category, only 14-methypentandecanoic acid, a 16-carbon fatty acid, was present in both BSs. This molecule was the main fatty acid present in L. jensenii P6A BS, representing 69% of the lipid fraction, while eicosanoic acid (47.43% of the lipid fraction) characterized L. gasseri P65 BS. Furthermore, galactose, glucose, and ribose were present in both the molecules in different percentages, even if rhamnose is peculiar of L. jensenii P6A. The antimicrobial activity against different potential human urogenital tract pathogens showed similar minimum inhibitory concentration (MIC) values for the two isolated BSs: 16 μg ml 𠄱 for E. coli and 128 μg ml 𠄱 for Klebsiella pneumoniae, Enterobacter aerogenes, and Staphylococcus saprophyticus. Interesting is the antifungal activity against the potential vaginal pathogen Candida albicans ATCC 18804, which was inhibited at a concentration of 16 μg ml 𠄱 . Furthermore, the biomolecules exhibited an antibiofilm activity showing the best result against E. aerogenes (its biofilm was disrupted for 64%).

Sambanthamoorthy et al. (2014), Cornea et al. (2016), and Merghni et al. (2017) reported the production of cell-associated antimicrobial BSs from different Lactobacillus strains, without any structural characterization. Lactobacillus casei produces two cell-associated BSs, named BS-B1 and BS-Z9 with an antioxidant activity (Merghni et al., 2017). At a concentration of 5.0 mg ml 𠄱 , BS-B1 and BS-Z9 BSs showed 74.6 and 77.3% of α-diphenyl-β-picrylhydrazyl (DPPH) radical scavenging activity, respectively. Furthermore, the antiproliferative potential on human epithelial cells HEp-2 after 48 h showed calculated values of IC50 that ranged from 109.1 to 129.7 mg ml 𠄱 . Moreover, the antiproliferative effect of BSs was directly proportional to its concentration indeed, at the maximum BS-B1 and BS-Z9 concentration of 200 mg ml 𠄱 , the antiproliferative levels were 67.19% and 66.72%, respectively. The antimicrobial and antiadhesive activities were evaluated only against S. aureus strains (the reference strain ATCC 6538 and the oral strains 9P and 29P). BS-LZ9 showed an antibacterial effect against the ATCC 6538 strain, while BS-B1 was effective against the oral pathogens 9P and 29P, showing IC50 values of 1.92 and 2.16 mg ml 𠄱 , respectively. However, the ATCC strain was more susceptible to the displacing (80.87�.86% of inhibition) rather than 29P strain (48.74�.84%) at a concentration of 12.5 mg ml 𠄱 . The antiadhesive capacity was maintained at the lowest concentration (1.56 mg ml 𠄱 ) since both BSs inhibit the adhesion of S. aureus ATCC 6538 and 9P of almost 50%. The antibiofilm potential was effective also on pre-formed biofilms.

Cornea et al. (2016) isolated Lactobacillus plantarum L26, L. plantarum L35, and Lactobacillus brevis L61 from Romanian traditional fermented food for the ability to produce BSs. Their antimicrobial and antifungal activities were evaluated against microorganisms having a role in food contamination or spoilage. All the extracted cell-bound BSs could inhibit E. coli growth, while a limited inhibition effect was observed by the L61 strain BS against Bacillus cereus. No effect was evidenced against S. aureus, yeast, and fungi. However, the BSs were able to inhibit the mycotoxigenic fungi sporulation, without affecting the mycelial growth that was justified assuming a non-optimal BS concentration.

Finally, Sambanthamoorthy et al. (2014) focused on L. jensenii and Lactobacillus rhamnosus able to inhibit clinical multidrug-resistant (MDR) strains of Acinetobacter baumannii (AB5075 and AB5711), E. coli EC433, and S. aureus strains [methicillin-resistant S. aureus (MRSA), clinical isolate 243, and UAMS-1]. Their crude BS extracts were effective against the MDR pathogens at a concentration of 50 mg ml 𠄱 . The best inhibition was due to L. rhamnosus molecule whose activity suppressed A. baumannii growth of 96�%, S. aureus UAMS-1 and MRSA strains between 80 and 93%, and E. coli of 72�%. These BSs also showed antibiofilm potential in a range of 25 to 50 mg ml 𠄱 . At the maximum concentration, A. baumannii and E. coli could not produce biofilm, while the ability was unpaired at lower concentrations for S. aureus. In order to use these biomolecules for biomedical applications, the cytotoxicity was tested against human A549 lung epithelial cells with different BS concentrations (from 25 to 200 mg ml 𠄱 ) for 24 h. Both biomolecules were a little bit toxic at the maximum concentration, while they were safe from 25 to 100 mg ml 𠄱 .

Among other bacteria belonging to the Firmicutes phylum, an antimicrobial cell-bound BS was isolated from the lactic acid bacterium Pediococcus dextrinicus SHU1593 (Ghasemi et al., 2019). BS yield of 0.7 g L 𠄱 was obtained when the strain grew on three substrates including a modified MRS medium (where glucose was replaced by lactose and Tween 80 was not present) and two low-cost materials such as molasses and date syrup. The BS solution at a CMC of 2.7 mg ml 𠄱 showed the minimum ST of 39.01 mN m 𠄱 . The chemical characterization pointed out its lipoprotein composition with around 52% (w/w) and 47% of lipid and proteins content, respectively (the remaining 1% corresponds to sugars, but the authors attributed this portion to the precipitated culture medium). The predominant fatty acids were oleic (60.28%), palmitic (25.08%), stearic (7.43%), and lauric (4.60%) acids. The BS composition was not dependent on the growth media thus, they all had similar nature, which was comparable with lipopeptides produced by members of Bacillus genus. At a concentration of 25 mg ml 𠄱 , Pediococcus BS inhibited E. coli, E. aerogenes, and Pseudomonas aeruginosa growth. However, the biomolecule was not active against Gram-positive bacteria such as B. cereus and S. aureus. Nevertheless, an important antiadhesive activity was evidenced against B. cereus (70.5%), P. aeruginosa (61.84%), and Salmonella typhimurium (58.69%).

Biosurfactants Released by Bacteria in the Surrounding Environment

Most of the BSs with an antimicrobial activity produced by bacteria associated with human health are molecules in the class of BSs released in the surrounding environment belonging to Firmicutes and Proteobacteria phyla (Supplementary Table 1). Understanding their characteristics, mechanisms of action, and their release might help to elucidate the relationships between bacteria�teria and bacteria𠄾nvironment. Consequently, this knowledge brings along the advantage of the high biotechnological potential. To date, the human-associated antimicrobial BSs described in the literature are included in the following chemical types: lipopeptides, glycolipids, glycoproteins, and glycolipoproteins.

Lipopeptide Biosurfactants

A proteinaceous nature is widely common among the molecules with an antimicrobial activity. For example, several antibiotics or bacteriocins have a protein nature, as well as the antimicrobial molecules released by the human body or by other cells.

Therefore, the importance of studying the protein domain through a genome-based or molecular approach for the prediction of the antimicrobial potential is clear, as evidenced by NRPS and PKS gene families (see section “Prediction of Biosurfactant With an Antimicrobial Activity by An “-omic” Approach”).

Some BSs with a proteinaceous nature have an antimicrobial potential against Gram-negative and Gram-positive bacteria, and several have also antifungal activities principally against Candida spp. Numerous authors reported the potential of cell-released BSs as antimicrobial, antifungal, and antibiofilm agents (Gudina et al., 2010 Gomaa, 2013 Perez et al., 2017). Among members of Lactobacillus genus, only two research studies report strains able to release antimicrobial lipopeptide BSs (Abdalsadiq et al., 2018 Emmanuel et al., 2019).

The first study reports the bioactive potential of the lipopeptide fraction compared with the glycolipid fraction isolated from the cell cultures of L. acidophilus and Lactobacillus pentosus against several antagonists such as Proteus mirabilis, S. aureus, Streptococcus pneumoniae, K. pneumoniae, and C. albicans (Abdalsadiq et al., 2018). The inhibition measured by the agar well diffusion assay (AWDA) on the extracted BS resulted in haloes ranging from 14.00 mm (against K. pneumoniae) to 44.00 mm (against S. aureus). The quantification of the MIC revealed that the lipopeptide fraction had a stronger antimicrobial effect at lower MIC values ranging from 7.81 μg ml 𠄱 (against P. mirabilis) to 62.5 μg ml 𠄱 (against K. pneumoniae), whereas glycolipid fraction from 15.6 to 62.5 μg ml 𠄱 . Furthermore, the antiadhesive activity against all pathogens showed inhibition percentages ranging from 65% (against P. mirabilis at a concentration of 250 μg ml 𠄱 ) to 93% (against K. pneumoniae at a concentration of 250 μg ml 𠄱 ) depending on the concentration of the lipopeptide fraction, while the antiadhesive activity of the glycolipid fraction produced a smaller percentage of inhibition (from 45 to 72.7%). Finally, the antibiofilm capacity of the molecules was demonstrated at a concentration of 250 μg ml 𠄱 , whose effectiveness was up to 100%. Specifically, the lipopeptide fraction evidenced the maximum antibiofilm percentage against K. pneumoniae and P. mirabilis and the lowest against S. aureus (85%).

Another example of antimicrobial lipopeptide BS produced by lactobacilli is the one from a Lactobacillus sp. strain isolated from homemade curd, yielding 3.21 g L 𠄱 (Emmanuel et al., 2019). It was characterized by the presence of alkene, alkyne groups, and conjugated diene and an emulsification index (E24) of 58.1%. The antimicrobial and antibiofilm activities of the BS were tested only against those of E. coli. The first showed a comparable antimicrobial activity with respect to sodium dodecyl sulfate (SDS), and the BS inhibited the biofilm of E. coli. Indeed, after 6 h, the number of E. coli cells forming the biofilm was lower as the lipopeptide concentration increased.

Undoubtedly, one of the most well-known lipopeptide BS producers are members of the Bacillus genus (Zhao et al., 2017). Several strains are employed as probiotics because of the formation of spores that survive in extreme conditions, such as low gastric pH. Once in the intestine, spores can germinate thus, Bacillus strains grow and re-sporulate, exerting an antimicrobial activity and other beneficial effects. However, nowadays, the use of Bacillus species as probiotics is disputed due to the capability of transferring genes for the antimicrobial resistance to the microbial population. Furthermore, the production of enterotoxins and biogenic amines by Bacillus strains is reported (Lee et al., 2019).

Nevertheless, helpful metabolites such as the antimicrobial lipopeptide BSs can be produced by members of the genus. For instance, a miscellaneous of surfactin lipopeptides was isolated from B. subtilis and Bacillus amyloliquefaciens supernatants after 24 h of fermentation on Malaysian fermented food: soybean known as tempeh showed a maximum surfactin yield at 84.08 mg L 𠄱 and cassava tapai the lowest at 26.9 mg L 𠄱 (Isa et al., 2020). However, the antimicrobial activity of the soybean BSs was not effective against S. aureus, S. pneumoniae, Serratia marcescens, and S. typhimurium, while the BSs from tapai inhibited the growth of both Gram-positive and Gram-negative tested bacteria. The most antimicrobial surfactins were produced by the growth on fish sauce budu showing a great inhibition halo against B. cereus (MIC 10 mg L 𠄱 ) and S. pneumoniae (MIC 25 mg L 𠄱 ) and a moderate one against Listeria monocytogenes (MIC 25 mg L 𠄱 ), S. aureus (MIC 25 mg L 𠄱 ), K. pneumoniae (MIC 25 mg L 𠄱 ), and S. marcescens (MIC 50 mg L 𠄱 ). Interestingly, Isa et al. (2020) confirmed the surfactin-producing ability of the strains through the detection of the sfp marker gene as well as the genus affiliation.

Ultimately, Schlusselhuber et al. (2018) reported Pseudomonas strain UCMA 17988, isolated from raw cow milk, for its ability to produce lipopeptide BS, although Pseudomonas spp. are famous for rhamnolipid production (Pornsunthorntawee et al., 2010). The maximum yield of 47.6 mg L 𠄱 was obtained after 4 days of cultivation. Interestingly, four molecules were identified differing at 14 Da, which suggested the presence of several lipopeptide isoforms. The hypothesis was confirmed by analyzing the differences due to the fatty acid chain: the major isoform was at 1,409 m/z, and the three other isoforms were detected at 1,381, 1,395, and 1,423 m/z. Therefore, the lipopeptide BSs were called “milksin” A, B, C, and D. The antimicrobial activity of the major isoform was observed against S. aureus CIP 53.154 with MIC of 0.5 mg ml 𠄱 , against L. monocytogenes WSLC 1685, and Salmonella enterica Newport CIP 105629 with MIC of 1 mg ml 𠄱 . Also, the antifungal activity was observed against strains representative of fungal groups: Mucor hiemalis CBS 201.65, Aspergillus niger CMPG 814, and Cladosporium herbarum CMPG 38 showed a major MIC of 20 mg ml 𠄱 , and Penicillium expansum CMPG 136 showed a MIC equal to 20 mg ml 𠄱 .

Glycolipid Biosurfactants

Glycolipids are complex molecules composed of a carbohydrate moiety and a lipid fraction. Although Pseudomonas spp. are the most prominent strains reported in the literature as glycolipid BS producers, also Gram-positive bacteria provide the same type of compounds that are released in the environment, for example, microorganisms grouped in the Lactobacillus genus.

Lactobacillus acidophilus NCIM 2903 is reported to produce a glycolipid type BS in 72 h of fermentation (obtaining 1.5 g L 𠄱 ) (Satpute et al., 2018). Indeed, its chemical characterization revealed the following principal functional groups: hydrocarbon, OH stretching, ester bonds, and sugars. The CMC was 625 μg ml 𠄱 , which corresponds to a reduction of the ST from 72 to 27 mN m 𠄱 . At the CMC value, the glycolipid inhibited 87% growth of S. aureus NCIM, 85% of P. aeruginosa MTCC 2297, 82% of B. subtilis MTCC 2423, 80% of E. coli NCIM 2065, 70% of P. putida MTCC 2467, and P. vulgaris of NCIM 2027. Satpute et al. (2018) utilized an innovative approach mimicking the biofilm microenvironment through microfluidic strategies to evaluate the antibiofilm property that showed no biofilm in the presence of the BS.

Also, Lactobacillus helveticus M5, isolated from yogurt, releases a glycolipid, characterized by a cycle aliphatic structure of the lipidic moiety when cultivated on lactose (5.5 g L 𠄱 yield in 120 h) (Kadhum and Haydar, 2020). It displayed an E24 of 75.3% and a reduction of the ST until 33.2 mN m 𠄱 . Its antimicrobial bioactivity was prevalently against Gram-positive bacteria than Gram-negative bacteria, showing an inhibition halo ranging from 15 to 31 mm against S. aureus and from 12 to 29 mm against P. aeruginosa at a concentration of between 20 and 100 mg ml 𠄱 . Thus, the authors speculated that the glycolipid could interfere with the peptidoglycan layer of the Gram-positive bacteria, leading to dysfunctions of the cell wall. Besides, the glycolipid acted as an antiadhesive agent at a concentration of 50 mg ml 𠄱 , inhibiting 78% and 74.5% of the adhesion of S. aureus and P. aeruginosa, respectively.

Among the gut commensal bacteria, Enterobacter cloacae B14 produced a glycolipid-like molecule releasing 39.8 mg BS (g cell dry weight) 𠄱 when yeast extract is used as a substrate. Its antimicrobial action was more pronounced against Gram-positive bacteria (inhibition haloes 20.7�.7 mm against B. cereus, B. subtilis, and S. aureus) with respect to the Gram-negative bacteria (9.7� mm against E. coli, P. aeruginosa, and S. marcescens). Interestingly, the BS was more effective than the commonly used antibiotic tetracycline against B. subtilis (respectively 22 vs. 20 mm of growth inhibition), and the BS inhibited the growth of the tetracycline-resistant strain S. marcescens (Ekprasert et al., 2020).

As already mentioned, P. aeruginosa is the most studied bacterium for rhamnolipid production. These molecules are formed by a rhamnose moiety linked to an aliphatic variable chain with a BS property. Different rhamnolipids exhibit an antimicrobial activity, such as the ones released by P. aeruginosa CR1 (Sood et al., 2020 Wahib et al., 2020).

Pseudomonas aeruginosa CR1 BS showed considerable antimicrobial and emulsification activities indeed, the E24 was 53%, and ST decreased until 35 mN m 𠄱 (Sood et al., 2020). It was recovered after the strain grew on both Luria Bertani (LB) broth supplemented with glycerol and basal medium enriched with rice bran oil, showing a maximum production of 10 g L 𠄱 . The chemical analyses revealed that P. aeruginosa strain CR1 produced only mono-rhamnolipids and that no di-rhamnolipids were detected. These data were confirmed by genome analyses showing the lack of rhlC gene coding for the rhamnosyl transferase responsible for di-rhamnolipid synthesis (Figure 2C and Table 1).

Wahib et al. (2020) evaluated P. aeruginosa strain, isolated from a clinical source, for its capacity to release 20.04 g L 𠄱 of antimicrobial BS when grown on glycerol medium. The BS was characterized as a mixture of mono- and di-rhamnolipids with E24 of 88.18%. Interestingly, at a concentration of 0.5 or 1 g ml 𠄱 , its rhamnolipids could inhibit E. coli, K. pneumoniae, and S. aureus growth, showing the maximum antimicrobial effect against S. aureus.

Glycoprotein Biosurfactants

Intriguingly, from literature retrieval, glycoproteins with antimicrobial and BS features are produced only by the Lactobacillus genus. Mouafo et al. (2018) investigated the potential of three Lactobacillus strains (Lactobacillus delbrueckii N2, Lactobacillus cellobiosus TM1, and L. plantarum G88) to produce BSs during growth on sugar cane molasses or glycerol. Their yields ranged between 2.43 and 3.03 g L 𠄱 on sugar cane molasses (with E24 ranging between 49.89 and 81%) and from 2.32 to 2.82 g L 𠄱 on glycerol (with E24 ranging from 41.81 to 61.81%). The molecules produced from the growth on glycerol were composed of a bigger fraction of lipids with respect to the BS obtained on sugar cane molasses. This suggested that lactobacilli could direct the glycerol in the lipolytic pathway and gluconeogenesis, consequently generating more lipids. The growth of L. cellobiosus TM1 and L. delbrueckii N2 on sugar cane molasses led to producing glycoproteins without a lipid fraction. The measured protein and sugar content were, respectively, 52.93 g/100 g MS and 27.10 g/100 g MS for L. cellobiosus TM1-BS, and 63.64 g/100 g MS and 51.13 g/100 g MS for L. delbrueckii N2-BS. Since the presence of sugars is independent of the carbon source (sugar cane molasses or glycerol), the authors speculated that the hydrophilic substrates were broken down in glycolytic pathway intermediates, such as glucose-6-phosphate, which is the precursor carbohydrate found in the BS composition. The antimicrobial effect indicated that Gram-positive bacteria were more sensitive than Gram-negative. As an example, Bacillus sp. BC1 growth was the most affected by the action of L. delbrueckii N2 glycolipid BS showing 57.5 mm of inhibition zone.

Glycolipoprotein Biosurfactants

Likewise, the production of glycolipoprotein BS was recorded only from two Lactobacillus strains, L. plantarum G88 and Lactobacillus paracasei subsp. tolerans N2 (Hippolyte et al., 2018 Mouafo et al., 2018), although these complex molecules are often cell-bound because of their big dimensions (see the section �ll-Associated Biosurfactants”).

Briefly, L. plantarum G88 growth on sugar cane molasses produced a molecule characterized by 8.96 g/100 g MS proteins, 51.13 g/100 g MS sugars, and 39.60 g/100 g MS lipids (Mouafo et al., 2018). Distinguishing an antimicrobial activity from that of E. coli E6, P. putida PSJ1 and PSV1, and Salmonella sp. SL2 was evidenced by the diameter of their inhibition haloes of 32.00, 32.00, 32.00, and 41 mm, respectively.

Curiously, Hippolyte et al. (2018) exploited L. paracasei subsp. tolerans N2’s ability to release bioactive compounds during growth on sugar cane molasses to evaluate the optimization of the production of an antimicrobial BS through a mathematical model. The model outputs were the predicted production yield and two values indicating the BS properties: the diameter of growth inhibition, a measure of the antimicrobial potential, and the ST related to the surfactant effect. After the fermentation under the optimal conditions (temperature between 33ଌ and 34ଌ, sugar cane molasses concentration ranging from 5.49 to 6.35%), they obtained an active BS with an experimental ST around 37.02 mN m 𠄱 , which was comparable with the predicted value (36.65 mN m 𠄱 ). The best glycolipoprotein production conditions for the highest antimicrobial activity comprised the lowest percentages of molasses (5.49%) and the lowest temperature (33ଌ). The measured inhibition halo against P. putida PSJ1 was 63.89 mm, which was comparable with the predicted one (62.07 mm). Then, the antimicrobial activity was assessed against other bacteria: P. aeruginosa PSB2, Salmonella sp. SL2, E. coli MTCC 118, Bacillus sp. BC1, and S. aureus STP1. S. aureus and Bacillus were the most sensitive bacteria to the glycolipoprotein with a MIC of 3.2 mg ml 𠄱 , while Salmonella and E. coli were the less sensitive with a MIC of 12.80 mg ml 𠄱 . Subsequently, a partial chemical characterization revealed that the main constituents were proteins, sugars, and lipids (63.64 g/100 g DM, 35.26 g/100 g DM, and 1.10 g/100 g DM, respectively), suggesting a glycolipoproteins nature.

Other Cell-Released Biosurfactants

Some antimicrobial BSs related to bacteria associated with human health were described for their bioactive properties without an exhaustive chemical elucidation or in few cases, the assembled chemical features make them part of new BS categories.

Although not characterized in-depth, the following examples showed the importance of BS properties for clinical, health-related, and nutrition problems and future applicative developments.

Foschi et al. (2017) focused the attention on the anti-gonococcal potential of Lactobacillus strains isolated from healthy premenopausal women. They principally belong to three different species: Lactobacillus crispatus, L. gasseri, and Lactobacillus vaginalis among which L. crispatus strains showed the best anti-Neisseria gonorrhea effect. In fact, their supernatant was able to eradicate N. gonorrhea viability after 7 and 60 min, while L. crispatus and L. gasseri species were capable only after 60 min. The most effective was produced by L. crispatus BC1, also possessing a potent BS property. The characterization of the molecules released in the supernatants indicated that their molecular weight was more than 10 kDa.

The BS extracted from Pseudomonas synxantha NAK1 stands out for its interesting biomedical application (Mukherjee et al., 2014). Indeed, the strain, isolated from Mycobacterium smegmatis plate, inhibits the Mycobacterium growth, which is a non-pathogenic bacterium model for the study of tuberculosis caused by Mycobacterium tuberculosis (Yamada et al., 2018). P. synxantha NAK1 cultivation generated metabolites that were preliminarily characterized as a 15-carbon aliphatic chain with intermediate oxygen and a terminal allyl bond with surfactant properties. The antimicrobial potential against other bacteria was thoroughly elucidated. The activity was very low against E. coli DH5α and P. aeruginosa AKS9 (MIC 200 μg ml 𠄱 ) moderate against B. subtilis, Shigella sonnei NK4010, and S. typhimurium B10827 (MIC 100 μg ml 𠄱 ) high against S. aureus ATCC 25923, M. tuberculosis H37Rv, and BGC (MIC 50 μg ml 𠄱 ) and, finally, very high against two M. tuberculosis strains (mc 2 155 and H37Ra, MIC 25 μg ml 𠄱 ). Therefore, this kind of secondary metabolite produced by P. synxantha NAK1 could be useful as an anti-tubercular agent against the mycobacteria pathogens.

Within the Proteobacteria phylum, other Pseudomonas strains revealed promising antimicrobial BSs. P. aeruginosa ATCC 10145 provides up to 1 g L 𠄱 of BS, characterized by an ST lowering capacity of 40 mN m 𠄱 (from 72 to 32 mN m 𠄱 ). The BS has also antimicrobial and antifungal activities showing an effect against Sarcina lutea, Micrococcus luteus, and Bacillus pumilus and among the fungi, the effect was against Penicillium chrysogenum and C. albicans (El-Sheshtawy and Doheim, 2014).

Among the first paper published regarding the Lactobacillus genus within the considered decade (2010�), Gudina et al. (2010) described a BS extracted from L. paracasei ssp. paracasei A20, which was isolated from Portuguese dairy plant. The extracted molecule was tested against 18 microorganisms, including species associated with the oral cavity, pathogenic bacteria, yeasts, and skin-associated pathogenic fungi. The antimicrobial potential was observed vs. all the strains, and the growth inhibition was observed for around 67% of the microorganisms at 50 mg ml 𠄱 . Only the cariogenic Streptococcus mutans strains NS and HG985, P. aeruginosa, the yeast Malassezia sp., and the fungi Trichophyton mentagrophytes and Trichophyton rubrum were non-sensible to the BS molecule. Regarding the antiadhesive capacity, a BS concentration of 50 mg ml 𠄱 inhibited the non-pathogenic Lactobacillus reuteri and L. casei of 77.6�.8% and 56.5�.8%, respectively.

The work of Gomaa (2013) described 10 Lactobacillus strains isolated from Egyptian dairy products among which L. paracasei produced a BS with an antimicrobial activity against C. albicans, S. aureus, and Staphylococcus epidermidis. Therefore, the authors compared this capacity with that of L. paracasei A20. Results showed that the novel extracted BSs demonstrated more potent antiadhesive compounds with respect to A20 strain. However, the best antiadhesive potential was attributable to Lactobacillus fermentum bioactive molecule (84.69% of inhibition) (Gomaa, 2013).

Other BS molecules were produced by strains isolated from food matrices. Two L. plantarum strains, called L26 and L35, and L. brevis strain L61, isolated from a Romanian traditional fermented food, produced BSs with an antimicrobial effect only against E. coli (Cornea et al., 2016).

Another example of BS from food derivatives is the screening of BS-producing capacity of bacteria isolated from dairy products, breast milk, fermented shrimps, and fruits (Abdalsadiq and Zaiton, 2018). Among 160 bacteria and 70 randomly selected to test the BS activity, only 20 cell-free supernatants were positive to drop collapse test and oil spreading assay. Furthermore, only six of the isolates were able to reduce the water-surface tension, leading to an average reduction from 72.22 to 37.21 mN m 𠄱 . The antibacterial activity was evidenced only for nine cell-free supernatants. Among them, the isolate L. acidophilus Fm1 was the most effective because it could inhibit the growth of Pseudomonas fluorescence (33.4 mm of zone inhibition), S. typhimurium (30.4 mm), P. aeruginosa ATCC 2785 (29.7 mm), P. aeruginosa 14T28 (25.5 mm), and E. coli (20.2 mm) (Abdalsadiq and Zaiton, 2018).

Moreover, among the four L. plantarum strains (Is2, Is9, Is12, and Is13) isolated from plantain wine (Mbamvu, or banana wine), a typical African fermented beverage, one isolate showed interesting BS and antimicrobial features. It was able to strongly inhibit the growth of selected pathogens, such as E. coli (3.3 cm of growth inhibition halo), Shigella flexneri (4.2 cm), Salmonella sp. (3.3 cm), P. aeruginosa (3.5 cm), and S. aureus (4 cm) (Moukala et al., 2019).

The last research studies represent an important description of the properties of bacterial bioactive compounds related to food and beverage fermented matrices as beneficial products for people’s health and ultimately to raise knowledge about nutritional issues (Parthasarathi and Subha, 2018).

Self Check

Answer the question(s) below to see how well you understand the topics covered in the previous section.

Critical Thinking Questions

  1. Explain how glucose is metabolized to yield ATP.
  2. Discuss the mechanism cells employ to create a concentration gradient to ensure continual uptake of glucose from the bloodstream.
  1. Glucose is oxidized during glycolysis, creating pyruvate, which is processed through the Krebs cycle to produce NADH, FADH2, ATP, and CO2. The FADH2 and NADH yield ATP.
  2. Upon entry into the cell, hexokinase or glucokinase phosphorylates glucose, converting it into glucose-6-phosphate. In this form, glucose-6-phosphate is trapped in the cell. Because all of the glucose has been phosphorylated, new glucose molecules can be transported into the cell according to its concentration gradient.

What caused my change of heart in promoting the ketogenic diet for cancer patients?

It started with several long phone conversations and email exchanges I had with a friend who runs a clinic in Mexico who was adamant that the ketogenic diet did not work in healing cancer long term. This coincided with the recurrence of cancer in someone I knew who was promoting the ketogenic diet (as effective).

It appeared to have some positive short term results for some people (shrinking or slowing down tumors), but I was beginning to have some doubts about it working long term. This uneasiness persisted for many months and I could not shake it. So I finally made the decision to take down my very popular post and youtube video about it.

Then came the coup de grace from Dr. Nicholas Gonzalez MD in October 2013.
(Addendum: Dr. Gonzalez passed away suddenly and mysteriously in 2015.)

Dr. Gonzalez and his colleague Dr. Linda Isaacs MD have had remarkable success treating cancer patients with a non-toxic nutritional protocol that incorporates some of the principles of the late Dr. Max Gerson MD along with the late Dr. William Donald Kelley’s protocol which includes high doses of pancreatic enzymes and individualized diets depending on body type and cancer type. I have huge respect for them, not because of their theories, but because they are getting RESULTS, including reversing “incurable” stage four cancers. Two volumes documenting 112 of their successful case studies can be found here.

Dr. Gonzalez wrote an eight part article series for Natural Health 365 on the history and failure of the ketogenic diet for cancer. Dr. Gonzalez’s nutritional cancer treatment expertise is much deeper than ANYONE currently promoting the ketogenic diet for cancer, because unlike anyone else promoting it, he actually treats cancer patients with nutrition every day.

There are thousands of people out there who have healed cancer naturally. I meet natural survivors constantly and even share their stories on this site. Most natural cancer healing protocols involve a radical change of diet and lifestyle that includes “overdosing on nutrition” with juicing, lots of raw plant food, little to no animal food, supplements, and herbal cleanses along with detox protocols. Those are all time-tested methods validated by a large body of long-term survivors.

I know a lot of long-term natural survivors, but I don’t know of any long-term survivors who have used a ketogenic diet to heal.

And then there’s the science…

There are several studies where researchers implanted human gliomas into the bodies of rats (a completely unrealistic scenario) and reported that the rats put on a ketogenic diet lived longer. In one study, rats with human brain cancer implanted in their bodies lived 56% longer on a ketogenic diet combined with hyperbaric oxygen therapy. 󈬨% longer” sounds huge until you learn that the mean keto/oxygen therapy survival was 55 days compared to the control rats who lived 31 days. And all the rats still died of cancer.

In another study, rats with human brain cancer implanted in their bodies achieved complete remission when fed a keto meal replacement shake called KetoCal and treated with radiation. Rats treated with a ketogenic diet (KetoCal) without radiation only lived 5 days longer than standard diet rats.

In this pilot study, 16 patients with advanced cancer reported that the ketogenic diet had some improvements in their quality of life, but were not cured.

This 2012 study showed that tumors can use ketones for fuel. Hello!

A 2017 study published in Cell found that a genetic mutation called BRAF V600E allows cancer cells to use ketones to grow faster. This mutation is present in 50% of melanomas, 10% of colon cancers, 100% of hairy cell leukemias, and 5% of multiple myelomas.

This 2014 study found that a keto diet helped anti-angiogenic drug bevacizumab work a little better for glioblastoma in humans, but had no effect alone.

According to a 2015 review of the literature on the ketogenic diet for human glioma patients (32 case studies), “Prolonged remissions ranging from more than 5 years to 4 months were reported in the case reports. Only one of these patients was treated using KD as monotherapy. The best responses reported in the more recent patient series were stable disease for approximately 6 weeks.”

A 2018 study found that the ketogenic diet combined with PI3K-inhibiting drugs slowed tumor growth in mice better than the drug alone, but the mice given the ketogenic diet alone had accelerated progression of acute myeloid leukemia.

When asked, “Does the ketogenic diet beat chemo for all cancers?” on the Tim Ferris podcast episode #188, Dominic D’Agostino, PhD, one of the most recognized ketogenic diet researchers in the world, said the following:

‘”Absolutely not… A number of situations where the ketogenic diet may not be the preferred therapy for most cancers, I would say, leukemia, lymphomas, Hodgkin’s lymphoma, thyroid cancer, testicular cancer, if caught early prostate cancer, melanoma, breast cancer. All these cancers can be effectively treated with chemotherapy or radiation in some cases, and also brain tumors if it’s grade 1 or 2 tumor that’s not very metastsatic and is more localized then surgery, radiation, and chemo can be very effective.”

Notice he used the word “effective” twice. The word “effective” does not mean cure. It typically only means temporarily slowed growth or temporary tumor shrinkage. To put it in perspective, over 580,000 “effectively treated” cancer patients die in the U.S. each year. The sobering truth is the cancer industry has only improved the overall cancer death rate by 5% in the last 60+ years. “Ineffectively treated” is a more accurate and appropriate way to describe the current state of affairs, but I digress.

The ketogenic diet has repeatedly been shown NOT to heal cancer as a monotherapy in rodents or humans, which has prompted researchers including D’Agostino to continue tacking on more protocols in an attempt to make it more “effective”, like fasting, calorie restriction, ketone supplements, hyperbaric oxygen, IV therapies, hyperthermia, nutraceuticals and chemo and/or radiotherapy.

It is my opinion that patients undergoing all of the therapies described above would do far better on a mostly raw, organic, whole foods plant-based diet, than on a ketogenic diet. Why? Because I know lots of survivors, myself included, who have healed cancer with that exact dietary strategy. I’ve interviewed 60+ of them here.

In the absence of clinical evidence, the next best thing is anecdotal evidence.

Survivors are the true test. And until there is a substantial list of long-term survivors, I cannot in good conscience support the ketogenic diet as a viable diet for healing cancer.

I am perfectly ok with being proven wrong, and if so, will freely admit it, but it will be at least 10 years before we know if the keto diet really works for any type of cancer, long-term.

Having said all that, there is tremendous value in short-term ketosis. The natural process of ketosis induced by a 3-5 day water fast or the 5-day ProLon Fasting Mimicking Diet has powerful benefits in the body including autophagy, as well as stem cell activation and regeneration. Learn more about that in my interview with world-renowned scientist and longevity expert Dr Valter Longo here.

Addendum: Dr. Charles Majors, DC was an avid promoter of the ketogenic diet for cancer. He spoke right after me at a conference a few years ago and argued against my plant-based dietary approach from the stage. Sadly, the ketogenic diet he insisted cancer patients adopt did not work for him and he died of brain cancer in late 2016.

Here is a short interview with Jonathan Landsman of Natural Health 365, in which the late Dr. Nicolas Gonzalez MD explains why a ketogenic diet doesn’t work for cancer.

If you want to take a deep dive, Dr. Gonzalez masterfully dismantles the ketogenic diet for cancer in the lengthy article below. This is not a scientific rebuttal, quibbling over theories about Warburg, glycosis, cell respiration, and ATP, rather it is a thoughtful, well-reasoned reflection from a medical doctor who was in the trenches of nutritional cancer treatment for nearly three decades. His real world experience with patients, insider knowledge, historical perspective and common sense put him head and shoulders above the lab-rat researchers and theorizers, no offense guys/gals.

The following article, which first appeared on Natural Health 365, is highly recommended for anyone who wants perspective on the ketogenic diet vs. carbohydrate-rich therapies that involve lots of fruits and vegetables, juicing, etc.

Enter Dr. Nicholas Gonzalez.

In this initial article, I’d like to begin by making the point that the world of cancer research and cancer medicine is littered with the discarded theories and rejected therapies thought at one time to be the next promising miracle, the final answer to this perplexing and deadly disease. In my own professional lifetime, I have witnessed a number of cancer miracles come and go, sometimes in quite dizzying succession and at times with extraordinarily dazzling hysteria.

I remember one of the first, from 1980 when I was a first year medical student at Cornell in this case, it was, according to the press and the journals, the magic of interferon, an immune stimulant destined to bring cancer to its knees. Not too long afterward, interferon would turn out to be a bust, with its promise and fame rising and falling in roller coaster-like style.

I lived through a far more extraordinary situation just five years later. I had graduated medical school by that point and was living in Florida, finishing my immunology fellowship under Robert A. Good, MD, PhD, the famed “father of modern immunology” as he had been called.

It was late 1985 when the media broke the story about the next cancer miracle. I was sitting in my apartment overlooking beautiful Tampa Bay, when I read the initial front-page newspaper reports. Dr. Steven Rosenberg, already well-known as Ronald Reagan’s surgeon (the President had a malignant polyp), and a highly regarded basic science researcher running a section at the National Cancer Institute in Bethesda, Maryland, had just revealed to the world – at a press conference, as I remember – his preliminary pilot study results with a new immune modulator, interleukin-2, that would provoke an extraordinary media frenzy.

The initial pronouncements, released with such glowing enthusiasm, indicated that finally, yes finally, after so many disappointments we might actually be looking at a real, universal cancer cure. In both laboratory and preliminary human trials, interleukin-2 – like interferon before it, a natural product secreted by lymphocytes that stimulates other cancer-fighting immune cells into action – had performed almost magically against even the most aggressive of cancers, such as metastatic melanoma and metastatic kidney cancer.

News of Dr. Rosenberg’s “miracle” was everywhere, in the print media, on the local and national news, and in an extended Newsweek story appearing December 16, 1985, with white-coated Dr. Rosenberg on the cover peering intently at the world. The article, titled “Search for A Cure” in large bold print went on for six pages, accompanied by photos of Dr. Rosenberg, one with a patient, another as the serious scientist in the lab. Elaborate, colorful artwork illustrated the narrative, showing the intricate mechanisms of the immune system, and pinpointing interleukin-2’s ability, under the guiding hand of Dr. Rosenberg, to fight malignant disease.

A separate subsection headlined “The Rise of a Superstar, From Reagan’s surgery to the frontiers of research” chronicled the compelling life story of Dr. Rosenberg. You couldn’t buy better publicity than this.

At the end of this piece, the writers did include a brief section titled “Interferon: A Cautionary Tale,“ reminding readers of the hoopla five years earlier over that other immune modulator, which too had been all the rage in the cancer research world. The essay, following the main laudatory articles, began:

To some ears, last week’s exultation over interleukin-2 has a familiar but discordant ring. Something similar happened about five years ago with a substance called interferon, the “magic bullet” of cancer research, featured on magazine covers and in articles with titles like “To Save Her Life – And Yours.” … But by 1984 the magic bullet had misfired now the articles were called “The Myth of Interferon.”

Over the years, I had become particularly familiar with the interferon story since my boss, Dr. Good, had done much of the original research linking it to a possible anti-cancer effect.

By that point, I knew Dr. Good quite well: during my second year of medical school, Dr. Good, at the time a professor at Cornell and Director of the Sloan-Kettering Institute, had begun guiding my fledgling research career. In 1982, during my third year of medical school, to my dismay the powers that be at Sloan pushed him out rather unceremoniously.

Subsequently, he spent some time at the University of Oklahoma, where he was hired to set up a cancer research division, before moving to All Children’s Hospital in St. Petersburg, where again he established a cancer research-bone marrow transplant unit.

When the news of interleukin-2 first hit the press, I discussed this new “miracle” with Dr. Good, who had grown quite cautious after years of experience and having witnessed many similar announcements followed by the inevitable letdown in the research community.

“Look at the data, always look at the data,” he said, “not the media reports.” I followed his advice, tracked down and studied the actual clinical data, which I found surprisingly unimpressive. As I recall, in the first uncontrolled trial, of more than 100 patients entered only three seemed to have experienced any significant or lasting response.

In subsequent months, reports of enormous toxicity, even patient deaths began to filter through the research community, serving to temper the initial hysteria. And it wasn’t cheap, as miracles go – the very toxic drug was so potentially dangerous it had to be administered in a hospital setting under very close supervision, with costs running in excess of $100,000 for a several-week course of treatment.

Despite the initial warning signs, the media continued its relentless promotion of interleukin-2 for a number of years. In 1992, perhaps due to political pressure more than scientific evidence, the FDA approved the drug for use against cancer, despite the lack of comprehensive controlled trials. Then in the late 1998 a clinical study – completed some 13 years after the initial reporting – showed that interleukin-2, at least with advanced kidney cancer, worked no better than placebo.

It’s still being used, though increasingly rarely, and no one I know talks about it with much enthusiasm.

By the 1990s, just as practicing oncologist were giving up on interleukin-2, bone marrow transplant (BMT) as a solution to poor prognosis or metastatic breast cancer started grabbing the headlines, touted as a cure for this most invidious of diseases striking so many women in the prime of life. Despite the lack of any compelling evidence it worked for this indication, bone marrow transplant was being pushed as a solution to deadly forms of breast malignancy. However, initially insurance companies refused to pay for this unproven and very expensive treatment, which could cost in those days up to $500,000 or more.

Nonetheless, enthusiastic oncologists joined with the media, portraying insurance companies as heartless, greedy bullies depriving women with breast cancer of a curative treatment. Not too long after, the trial lawyers got involved, orchestrating a series of lawsuits against various insurance companies on behalf of women wanting a BMT. In a particularly notable and telling case, Fox vs. HealthNet, the jury awarded the plaintiff, a woman diagnosed with breast cancer whose insurance carrier refused to cover the procedure, $89 million, including $77 million in punitive damages.

Under such threat, the insurance industry relented, finding it cheaper to pay the $100,000 or $200,000 or $500,000 per procedure then risk such catastrophic financial harm.

After some 40,000 women underwent the procedure – at a time when 10-30% of patients died from the treatment itself – it was eventually proven to be worthless. The one glowing positive study from 1995, the infamous South African study of Dr. Bezwoda, turned out on closer examination to be a complete fraud, with the creative researcher simply making up the data. The wonderful and frightening book False Hope describes the bone marrow transplant-breast cancer fiasco in great detail, for those with an interest.

As these battles waged in the early 1990s, I had long left Dr. Good’s group, having returned to New York and private practice. Nonetheless, this story had a personal ring to it, as had the interferon story, since Dr. Good had completed the first bone marrow transplant in history, in 1969, and long hoped this technology would be, yes, an answer to cancer.

Under his direction, during my fellowship years I learned how to do this very tricky and often deadly procedure.

But no fear, there’s always a new miracle around the corner, and in 1998 the newspaper reporters and TV newscasters, having effortlessly drifted away from interferon and interleukin-2 and the bone marrow transplant craze, were all in a tizzy over the newest “final” solution to cancer, anti-angiogenesis, based on the pioneering work of the late Dr. Judah Folkman of Harvard. Dr. Folkman had spent decades studying the process of angiogenesis in cancer tissues, the formation of new blood vessels that allow tumors to grow quickly and invade through normal tissues and organs with deadly effect.

Without a rich blood supply, cancerous tumors cannot grow beyond a cubic centimeter.

Dr. Folkman had developed two drugs, angiostatin and endostatin, that in animal experiments reversed tumor growth by blocking new blood vessel formation, essentially starving out the cancer cells. In a November 1998, presentation of his work at the National Institutes of Health in Bethesda, Maryland, Dr. Folkman announced to the world that at least in mice, “we have not seen a tumor we cannot regress.”

Though Dr. Folkman’s research was all based on laboratory experiments and animal studies, the powerful NCI publicity machine took up the cause, with the smell of “miracle” again in the air, despite the lack of any evidence that Folkman’s anti-angiogenesis drugs worked against human cancer. Nonetheless, with the NCI and NIH on board, the media, large and small, local and national, seemed transported into a state of frenzy.

I recall so well, this time sitting in my mid-Manhattan office, reading that famous May 3, 1998 front page lead New York Times article (in the upper left of the page reserved for wars, revolutions, and, yes, miracles) by reporter Gina Kolata, announcing Folkman’s preliminary findings to the world, extolling anti-angiogenesis in a tone that one more skeptical writer, Jack Breibart, described as “breathless.”

Kolata quoted no less an authority than Dr. James Watson, the Nobel Laureate in 1962 for his discovery, with his colleague Frances Crick, of the structure of DNA, the basic genetic material. “Judah is going to cure cancer in two years,” Watson told Kolata. You couldn’t ask for a better source, making a more definitive claim.

Kolata’s unrestrained reporting continued: “Dr. Watson said Dr. Folkman would be remembered along with scientists like Charles Darwin as someone who permanently altered civilization.”

The writer also quoted an enthusiastic Richard Klausner, MD, at the time Director of the National Cancer Institute, who assured the world, “I am putting nothing on higher priority that getting this into clinical trials.”

The glowing TV stories followed, including a memorable prime time, one-hour special about the subject on ABC hosted by the late Peter Jennings. The other networks, in quick succession, picked up the cause. However, not too long after, word broke that Times’ reporter Kolata had been, through her agent, hawking to publishers an idea for a book about anti-angiogenesis and cancer.

Her agent, according to reports at the time, began circulating a book proposal the day after the Times story ran, asking for a $2 million dollar advance! The whole episode raised some eyebrows over a reporter seeking to benefit personally from a subject she was promoting in the news section of the Times. After a fair amount of criticism, Kolata withdrew her book proposal.

As Dr. Klausner promised, the National Cancer Institute, probably swept up in the national and international explosion of hope and enthusiasm, “fast tracked” a preliminary study of endostatin in human patients, intending to enroll, as I recall, 70 subjects very quickly.

But what surprised me – and what began to concern others I knew in the medical community – was some time later the deafening silence about the trial’s outcome, and what seemed to be a blackout about the actual data. Eventually, the study results were published indicating that 42 subjects had been ultimately recruited for the trial, not the planned 70, and not a single one of these had responded to the drug.

Ironically Jennings himself, who had promoted the therapy with unabashed enthusiasm, would die of lung cancer, only months after his diagnosis in 2005. Folkman too, has passed on, never to realize his hope of an anti-angiogenesis, cancer-free world.

Nevertheless, anti-angiogenesis as the answer to cancer remains a big driving force in “biotech” companies, who have developed a whole slew of angiostatin and endostatin offspring, including the drug Avastin, costing up to $10,000 a month, though it doesn’t work particularly well. The clinical studies aren’t impressive, usually reporting several months of improved survival in patients diagnosed with a variety of advanced cancers.

In a further ironic turn, in December 2010, after approving the drug for treatment of women diagnosed with breast cancer, the FDA rescinded its blessing of Avastin for this indication when clinical trials failed to show any significant benefit.

The anti-angiogenesis love affair not only affected conventional researchers and oncologists, but infiltrated deeply into the “alternative” cancer world. During the late 1990s, I read numerous articles lauding the anti-angiogenic effect of various herbs. Some ten years ago or more, a number of alternative physicians began promoting artemesinin, an herb from Africa long used as a treatment for malaria, as a “natural” anti-angiogenesis supplement.

But ten years after the initial burst of enthusiasm, few of my colleagues even mention it.

And so it goes. We as a culture, as a nation, as a world, are forever looking for miracles from our scientific and medical gurus, miracles that might finally bring cancer to its knees. And there will forever be miracles ripe for the picking.

In 2012, Dr. Thomas Seyfried, a PhD basic science researcher, published the book, Cancer as a Metabolic Disease, announcing to the world that a high-fat, no carbohydrate ketogenic diet represents the solution to cancer prevention as well as to cancer treatment. His monograph has been greeted with much acclaim, though not yet at the level reached at the height of the interleukin-2 hysteria in 1985.

Dr. Seyfried, whom I do not personally know, is hardly an “alternative” medical scientist, since judging by his credentials listed on the back cover of the book his pedigree seems conventionally academic:

THOMAS N. SEYFRIED, PHD, has taught and conducted research in the fields of neurogenetics, neurochemistry, and cancer for more than twenty-five years at Yale University and Boston College. He has published more than 150 scientific articles and book chapters …

A closer look at Dr. Thomas Seyfried and his work

Certainly Dr. Seyfried has put together a most impressive achievement, chronicling in great detail his belief that cancer does not develop from genetic alterations – as is generally believed – but as a result of changes in fundamental cell physiology, specifically changes in energy production, that in turn lead to the cancer phenotype. In essence, the genes remain intact, but metabolism goes awry.

The book summarizes, then enlarges upon, the concepts of Otto Warburg, MD, the great German scientist who won the Nobel Prize in Medicine and Physiology in 1931 for his work on cellular oxidation and energy production. No scientist has ever been nominated more frequently for the cherished Prize than Dr. Warburg, but he lost his chance for a second win, according to some sources, in 1944 after Hitler ordered that no German scientist could accept the award.

Who is Dr. Otto Warburg?

To sum up decades of Warburg briefly, mammalian cells create and store usable energy in the form of the adenosine triphosphate (ATP) molecule. Production of ATP is a complex affair involving three distinct and sequential series of cellular reactions that begin with the breakdown of the six-carbon sugar glucose. The first of these processes, glycolysis, does not require oxygen and occurs in the cytoplasm the second, the citric acid cycle, occurs within the mitochondria, the oval shaped organelles dispersed within the cytoplasm, and requires oxygen and the third, and most productive in terms of ATP generation, electron transport, proceeds in the membranes of mitochondria and also needs oxygen.

In normal mammalian cells, glycolysis represents the starting point of energy synthesis. Its end product, pyruvic acid, is in turn shunted first into the citric acid cycle, then ultimately into the electron transport chain. Along the way, a complex series of step-wise reactions releases multiple energy-rich ATP molecules.

Based on his years studying cellular metabolism, Dr. Warburg proposed that cancer cells, unlike normal cells, rely exclusively on anaerobic glycolysis for energy. Such cells do fine in the absence of oxygen, since the metabolic machinery of glycolysis doesn’t require it.

Warburg claimed that in these abnormal cells glycolysis actually uncouples from the citric acid cycle and electron transport, leaving the cells dependent solely on this rather inefficient mechanism for survival. Bacteria also synthesize their ATP energy exclusively from glycolysis, in the process we know as fermentation.

This uncoupling of glycolysis from the citric acid cycle and electron transport, and the supposed fundamental dependency of cancer cells on anaerobic metabolism, has been studied extensively since Warburg’s day, with many scientists around the world claiming to confirm, then adding to, Warburg’s hypothesis. As Dr. Seyfried correctly points out, in more recent times, cancer researchers have begun drifting away from the study of disordered cellular physiology, enamored as they are of genetic abnormality as the primary and only driving force in cancer formation and growth.

Warburg’s ideas about faulty metabolism seem to have been overshadowed by the elegance of, and fascination for, the “genetic cause of cancer.”

I agree Dr. Seyfried has done us all a great service by redefining, re-emphasizing and refining Dr. Warburg’s remarkable research from 80 years ago. He makes the case, using the contemporary basic science data, to support Warburg’s belief that cancer cells depend solely on glycolysis for survival, with his claim regarding the uncoupling of this sugar-fueled, oxygen-independent process from the citric acid cycle and the electron transport chain. But he goes a major step further, stating as fact that since cancer cells depend on anaerobic glucose metabolism for energy, they can be stopped in their tracks by depriving them of blood glucose.

Our normal healthy cells, be they situated in the brain or the skin of our feet, do prefer glucose as their primary energy source, obtained from the sugar circulating in the blood. That “blood sugar” comes from a variety of sources, including dietary carbohydrates occurring in fruits, starchy vegetables like potatoes, and grains. The complex carbohydrates in such foods are broken down into glucose during the digestive process, catalyzed by a variety of carb-specific enzymes like amylase.

We also maintain a certain amount of stored sugar as glycogen, found in the liver and muscle and formed when glucose molecules link up to one another in complex chains. In times of need and if deprived of dietary carbohydrates, our liver and muscle cells can break down glycogen into glucose for release into the bloodstream. Our liver cells can also, when necessary, convert certain amino acids such as alanine into glucose.

However, our glycogen supplies in the liver and muscle are quite limited, providing only an 8-12 hour emergency supply. So during a fast, or starvation, or on a diet providing no carbohydrates in any form, we quickly run out of glycogen. In this situation, through a variety of neural and hormonal signaling, our fat cells, or adipocytes, begin releasing free fatty acids into the blood stream. These fatty acids can in turn be used by our cells in the alternate ATP producing process of beta oxidation.

The end result of this series of reactions, acetyl coenzyme A, can then be shunted into the citric acid cycle and the electron transport chain, to produce maximum amounts of energy-rich ATP.

Though most of our cells can utilize fatty acids of all stripes via beta oxidation to create ATP energy, our central nervous system is at somewhat of a disadvantage. In fact, long chain fatty acids with 14 or more carbons, which can yield the most ATP from beta oxidation, do not cross the blood-brain barrier. However, in a state of prolonged dietary carbohydrate depletion, the liver begins converting acetyl coenzyme A into various ketone bodies, such as acetoacetate and beta hydroxy butyric acid, which easily penetrate into the brain and which can, like acetyl coenzyme A, be shunted into the citric acid cycle and then the electron transport chain, providing the brain with ATP.

On a low carb or no carb diet, our billions of cells in all our tissues and organs switch their energy mechanics from a process driven by glucose to one propelled by fatty acids and ketone bodies. The term “ketosis” simply means the state in which, in the absence of sufficient glucose, our liver synthesizes ketones from acetyl coenzyme A.

However, even on a no carb, all meat, high-fat diet, we will still be consuming some glucose in the form of glycogen stored in muscle and organ meats, and our livers will continue to convert some dietary amino acids into glucose, so blood sugar levels never hit zero on such a diet. But in such cases, the amounts produced will be minimal.

Though our normal cells do just fine in the absence of carbohydrates, cancer cells, Dr. Seyfried claims, do not. These cells, he says, can never use fatty acids or ketone bodies for any significant energy production, since the citric acid cycle and electron transport in them remain basically inactive. So, he proposes, as the culmination of his exegesis, that on a high fat, moderate protein, no carb diet, a cancer patient will deprive his or her deadly abnormal cells of their only useful source of energy, blood glucose, leading to apoptosis, or cell death.

It’s that simple. No dietary sugar, no cancer.

The science is impressive, the conclusion, to many it seems, extraordinarily promising. But, is this ketogenic diet really a “new” idea or simply an old one, repackaged for the 21st century? And, can history teach us anything about its efficacy against cancer, or any other disease?

During the first half of the 20th century, physicians and researchers studying the traditional Eskimo (Inuit) culture were amazed by the health of these people subsisting on a very peculiar – at least to the Western academic mind – high fat ketogenic diet. The famed Arctic explorer Stefansson first documented the traditional Eskimo diet, which was later studied in some detail in the early 1930s by a research team from McGill University in Montreal.

To the surprise of these investigators – at the time no Western scientist believed any human could survive on nothing but meat – this Eskimo diet consisted of virtually 100% animal products, 80% in the form of fat, with much of it saturated, 20% protein, but essentially no carbohydrates. From cradle to grave these traditional Eskimos lived in a state of ketosis.

In retrospect, it makes sense that in the Arctic the Eskimos, in order to survive, would have adjusted to their high fat, moderate protein, no carb diet. With its brief summer and lacking soils suitable for crops, the region provides insufficient plant foods suitable for human consumption but does offer an abundance of fatty animal food both on land and in the sea. If the Eskimos hadn’t adapted to such food, living as they did in such a difficult, extreme part of the world, they simply would have died off.

Interestingly, as Stefansson pointed out, the Eskimos he studied and lived with for ten years knew that their exclusive animal food diet must be high fat, with moderately low protein. They warned a diet lacking sufficient fat (or as a corollary in Western scientific terms, high protein), would lead to sickness and eventually death.

As Stefansson and later scientists learned, the Eskimos living on their high fat, ketogenic diet seemed free from the typical degenerative diseases including cancer and heart disease, already becoming rampant in the Western world during the early decades of the 20th century. In 1960, the elderly Stefansson – was quite a celebrity by that time for his adventures to far away places – wrote a book entitled Cancer: Disease of Civilization?, in which he made the case that the typical Eskimo diet offered complete protection from this frightening malady.

In a number of his best-selling books, Stefansson argued strongly that we should all be living like Eskimos, indulging in high fat, moderate protein, no carb diets – that is, if we wanted superb, enduring good health.

Blake Donaldson, MD, who ran a general practice for decades on Long Island, New York, began prescribing a ketogenic diet in the 1920s. Donaldson, who was quite familiar with Stefansson’s reports on the Eskimo diet, began recommending an all-meat, high-fat regimen for his patients diagnosed with a variety of complaints such as obesity, diabetes, and heart disease, though he doesn’t appear to have treated cancer specifically. In his 1961 book, Strong Medicine, Dr. Donaldson summarized his findings and his many years of experience recommending a high fat diet.

More recently, the famed New York diet doctor, Robert Atkins, MD, popularized the ketogenic diet, not for cancer, but as the ultimate weight loss plan with his books over the decades selling in the tens of millions of copies. The original version of the Diet Revolution published in 1972 sold at one point more than 100,000 hard copies a week, in those days the fastest selling book in the history of United States publishing.

As the years passed, Dr. Atkins, a cardiologist by training, began to see in the ketogenic diet the answer to many of the problems of Western civilization beyond obesity, including heart disease, diabetes, hypertension – and yes, even cancer.

The traditional Atkins’ Diet was certainly high fat, in the range of 70% or more, nearly all from animal sources, and with minimal dietary carbs, less than 10%. Dr. Atkins, famed for his all-encompassing emphasis on ketosis during his early years as a diet doctor, insisted his patients routinely check the levels of ketone bodies in their urine several times a day, using special “ketone strips.”

In his books and in his office working with his own patients, Dr. Atkins warned that to reap the benefits of his diet, one must reach and stay in a state of ketosis, much like the traditional Eskimos. Even a slight deviation from the diet, some ill-advised cheating with a cookie or candy, could stop ketosis in its tracks, and with it, the value of the diet.

I knew Bob quite well, and considered him a friend. We first met when I interviewed him for a nutrition story during my journalism days, and later on while I was a medical student, we kept in close contact. During my freshman year at Cornell Medical School – from which Bob had received his own medical degree – I arranged for him to speak as part of a lecture series I had set up on alternative approaches to disease.

After I finished my conventional immunology training under Dr. Good, in 1987 Bob graciously offered me a job in his clinic, not to work with patients seeking dietary or general nutritional advice, but to help supervise a cancer unit he was then in the process of establishing. Though I was grateful for the proposal, I turned him down, determined to set up my own practice.

Bob had achieved great success as a diet doctor, with an estimated wealth at the time of his death in 2003 in the range of $350 million. He was also a very driven and very smart physician, who clearly saw in cancer, and not in obesity, the ultimate challenge in medicine.

Bob, who knew Stefansson’s work well, told me during more than one dinner together in the late 1980s that the ketogenic diet might represent the ultimate solution to cancer. He thought, as Donaldson and Stefansson had claimed before him, that all humans should be following a ketogenic diet to achieve ultimate ideal health. But were they right? Or was there another, perhaps more accurate way, to look at the human dietary condition?

Nathan Pritikin believed, and fanatically so, that all humans were genetically and metabolically programmed to follow a high carb, very low fat, exclusively plant-based diet, which if applied diligently would protect us from all the major degenerative disease killers, such as diabetes, heart disease, hypertension – and perhaps, even cancer.

The traditional Pritikin diet was literally a mirror image of the Atkins’ Diet, with about 70-75% of all calories derived from carbohydrates, 15-20% from protein, all from plant sources, and 8% or less from fat, again all plant-derived.

After Pritikin’s death in 1985, Dr. Dean Ornish of San Francisco would pick up the Pritikin mantle, eventually testing a similar diet in patients diagnosed with heart disease as well as in patients with prostate cancer.

The nutritional world then, as it is today, was surely confusing, with various scientists, physicians, and lay authors promoting one diet or another, often – as in the case of Atkins and Pritikin – offering completely contradictory dietary recommendations. Fortunately, when in 1987 Dr. Atkins offered me a job, I had already found what I thought represented a solution to the dilemma of dueling dietary dogma.

By the time I began medical school in 1979 I had read the pioneering work of Weston A. Price, DDS, the American dentist and researcher. Beginning in the late 1920s, Dr. Price, accompanied by his wife, spent seven years traveling the world evaluating isolated groups of people living and eating according to long-standing tradition. Today such a study would be impossible, since just about everyone everywhere has adopted the “Western” way of living and eating, down to jeans and junk food.

But in Dr. Price’s day, many groups living in many different locations still lived according to tradition largely untouched by modern Western influence. Price’s travels took him from the Eskimos of the Arctic, to the descendents of the Incas living in the high Andes, to the Masai on the plains of Kenya, to isolated Swiss herders in the Alpine mountain valleys, to Polynesians living on pristine tropical islands.

The variety of diets around the world

Each of these groups Dr. Price studied seemed well adapted to the available food supply. The Eskimos, as Stefansson earlier had reported and as Price confirmed, thrived on their high fat, no carb, animal-based diet. The Inca descendents, on the other hand, had done quite well consuming grains like quinoa, along with tubers, fruits, and some animal protein and dairy. The Masai flourished on a rather extreme diet consisting, for an adult warrior, of a gallon of raw milk a day with some blood and occasional meat, but no fruits, vegetables, nuts, seeds, or grains.

The Swiss herders did just fine living on raw pastured cow milk and cheese accompanied by a nutrient-dense, whole grain bread. The Polynesian diet centered around coconut in all its incarnations, the milk, meat, and cream, creatively used in a variety of ways, along with fish, some wild animal meat, and fruits. These diets could not be more different an Eskimo never drank milk or ate a coconut, the Inca descendents never saw a coconut or whale blubber, a Masai never ate coconut or grains, the Polynesians never consumed grains, never drank milk, and never ate cheese.

However different these diets might be, each of these groups, and the many other traditional peoples Price studied, enjoyed excellent enduring health, free from the diseases of civilization – cancer, diabetes, heart disease, and hypertension. In his extraordinary and very detailed 1945 book Nutrition and Physical Degeneration, Dr. Price documented his thesis that we humans over the millennium adapted to and thrived on not one, as the experts usually claim, but a variety of different diets.

There were some commonalities among the diets, of course all these traditional people ate some animal products, and all consumed a fair amount of fat, whether from plant or animal sources. All the food was, of course, locally grown, locally harvested, or locally hunted, since these isolated groups lacked access to the industrialized food of modern “civilization.”

The food had to be local. And all these groups ate some food in its raw, uncooked form, which they believed possessed special nutritional value.

Having first read Dr. Price’s book during my journalism days, I knew that according to his exhaustive work, humans were a varied species, in the past living in and adapting to all ecological niches excepting the Antarctic, offering a variety of food sources. To me, his work offered a solution to the conflicting dietary advice even then being offered to the world. It didn’t make sense as Nathan Pritikin insisted or as Bob Atkins argued, that all humans should follow one specific type of diet: It just didn’t seem reasonable, to me at least.

I would receive further support for my thinking during the summer of 1981, after completing my second year of medical school. That July, through one of my journalism contacts from my previous life, I had the opportunity to meet the controversial alternative cancer practitioner, the dentist Dr. William Donald Kelley. Over a 20 year period beginning in the early 1960s, Kelley had developed a very intensive nutritional approach to cancer that came under harsh public scrutiny and media attention when he agreed to treat Steve McQueen.

Steve McQueen was diagnosed with advanced mesothelioma, a particularly deadly form of cancer associated with asbestos exposure, sought out Kelley after the conventional approaches, radiation and immunotherapy, failed to halt the progression of his disease. Though he seemed to rally initially, McQueen, according to accounts of those involved with his care, was not particularly compliant, and appeared at the time he first consulted Kelley too sick for any therapy to work. He would eventually die at a Mexican clinic under the condemning gaze of the media for his choice of an alternative method.

My writer friend had been in touch with Dr. Kelley, thinking that with all the attention around him he might make a good subject for a successful book. But she wanted me to meet in person with Kelley, who happened to be in New York to discuss her book project. Frankly, as she explained to me, she needed my take on the man, whom she really couldn’t decipher – was he truly onto something useful and extraordinary with his odd therapy, or was he simply a huckster, taking advantage of vulnerable cancer patients, as the media had been insisting.

Though initially reluctant, I agreed to meet with Kelley, who turned out to be far different from what I expected. I found him to be very shy, very thoughtful, and clearly very smart. And, I could see that he was passionately devoted to his nutritional approach to cancer.

During that first meeting, Kelley described in some detail the tenets of his therapy. In summary, it involved three basic components: individualized diet, individualized supplement programs with large doses of pancreatic enzymes Kelley believed had an anti-cancer effect, and detoxification routines such as the coffee enemas. He fervently believed that each patient required a protocol designed for his or her particular metabolic, physiologic, and biochemical needs, and that one diet would never be suitable for all.

As I was to learn, the diets Dr. Kelley prescribed ranged from largely plant-based high-carb to an Atkins-like diet, with patients prescribed fatty meat several times daily. In general Kelley believed patients diagnosed with the typical solid tumors – cancers of the breast, lung, stomach, pancreas, colon, liver, uterus, ovary, prostate – did best adhering to a plant-based, high carb type diet, low in animal protein and animal fat.

Patients diagnosed with the immune based “blood cancers” like leukemia, lymphoma, and myeloma, as well as the sarcomas, a type of connective tissue malignancy, required a lower carb, high animal fat, moderate animal protein diet. Other patients, usually with problems other than cancer, thrived on a more “balanced” diet, incorporating a variety of plant and animal foods.

But all his patients ate some carbs in the form of fruit and carrot juice, the amounts allowed varying according to the underlying metabolic makeup. All this resonated with me, having studied the work of Weston Price so intently.

After my original lengthy conversation with Dr. Kelley, my research mentor Dr. Good suggested that during my summer break I begin an informal review of Kelley’s patient charts located in his Dallas office. From my first day in Dallas, I found among Kelley’s records patient after patient with appropriately diagnosed poor prognosis or what would be considered terminal disease such as metastatic pancreatic and metastatic breast cancer, who had done well under his care for many years, often with documented regression of his disease.

These preliminary findings spurred Dr. Good to encourage a more thorough investigation of Kelley’s methods and results. As the project grew in scope, I continued my “Kelley Study” in my spare time during the last two years of medical school, and ultimately brought it to completion while pursuing my immunology fellowship training under Dr. Good at All Childrens’ Hospital in St. Petersburg.

For the study I reviewed thousands of Kelley’s charts, interviewed over a thousand of his patients, and evaluated 455 of them in some detail. I eventually put my information into monograph form under Dr. Good’s direction, including 50 lengthy case reports of patients with 26 different types of appropriately diagnosed, poor-prognosis cancer who had responded to Kelley’s nutritional regimen.

One of these patients, a woman from Appleton, Wisconsin, had been diagnosed in the summer of 1982 with stage IV pancreatic adenocarcinoma, the most aggressive form of this most aggressive disease. A liver biopsy during exploratory surgery confirmed the diagnosis of metastatic cancer, which the Mayo Clinic would later confirm. When the Mayo oncologist on the case said there was nothing that could be done, the patient being looking into alternative approaches, learned about Kelley’s work, and began his therapy.

Thirty-one years later, she is alive and well, having seen her children – and now her grandchildren – graduate college. To put this case in perspective, I know of no patient in the history of medicine with stage IV pancreatic cancer and biopsy proven liver metastases who has lived this long.

Another memorable patient written up for the book had been diagnosed with what was thought to be localized endometrial cancer in 1969. After a course of radiation to shrink her large tumor, she underwent hysterectomy, and was told they “got it all.” Over the next few years, however, her health began to deteriorate: she experienced persistent fatigue, malaise, pelvic pain, and weight loss.

Though she returned to her primary care physician repeatedly, he dismissed her complaints as “nerves,” suggesting only a tranquilizer. Eventually, in 1975 she developed a palpable mass the size of a grapefruit in her pelvis, thought by her doctors – finally taking her seriously – to be an indication of obvious recurrent disease. A chest x-ray at the time revealed multiple nodules in both lungs, consistent with widely metastatic cancer.

Though told her situation was dire and her cancer incurable, she underwent surgery to remove the large pelvic tumor, to avoid an impending intestinal obstruction. Shortly afterwards she began a synthetic progesterone used at the time as a treatment for metastatic uterine cancer.

Her doctors admitted the drug would not be curative, but hopefully might extend her life a few months. However, she stopped the medication after a few weeks because of serious side effects, and with no other conventional options in sight she began looking into alternative approaches.

She learned about Kelley’s work, began the program, regained her health, and avoided all conventional doctors for many years. In 1984, nine years after coming under Kelley’s care, she returned to her primary care physician who was quite perplexed she was still alive after all this time. A chest x-ray showed total resolution of her once widespread lung metastases.

This patient eventually lived until 2009 when she died at age 95, having survived 34 years from her diagnosis of recurrent metastatic uterine cancer.

Although Kelley did prescribe a variety of diets for his cancer patients, these two exemplary patients followed a plant-based eating plan, high in carbohydrates with a minimum each day of four glasses of carrot juice, dense in nutrients but also dense in natural sugar. Each of these diets allowed considerable fruit and whole grain products, foods again loaded with carbs. According to Seyfried’s hypothesis, both should have died quick miserable deaths.

At the time I finished my monograph in 1986, I hoped that with its publication, fair-minded researchers might begin taking Dr. Kelley and his nutritional therapy seriously. As I was to learn, I completely and rather naively misjudged the animus of the scientific community toward unconventional cancer treatment approaches that didn’t fit the “accepted” model. Even with Dr. Good’s support, after two years of trying I could not get the book published, either in its entirety, or in the form of individual case reports appropriate for the conventional medical journals.

Editors responded with disbelief, claiming the results couldn’t be real since a non-toxic nutritional therapy could never be useful against advanced cancer. I found the logic, “it couldn’t be true because it couldn’t be true” perplexing, for editors of scientific journals. In any event, the book would finally be published, in a rewritten and updated form, in 2010.

Discouraged by our failure to get the results of my five-year effort into the world, in 1987 Kelley closed down his practice and more or less went off the deep end, disappearing from sight for a number of years. After we parted in 1987, he and I would never speak again.

In 2005, he would eventually die with his dream of academic acceptance unrealized. But my colleague Dr. Linda Isaacs and I have worked diligently over the past 26 years, keeping the Kelley idea alive, that different people may require completely different diets. In the next installment, I will address my own experience treating patients diagnosed with advanced cancer with a Kelley based approach. Our therapy involves, oftentimes, diets high in carbohydrates, which proponents of the ketogenic diet would predict should fuel, not stop, cancer.

After Kelly closed down his practice, in late 1987 I returned to New York and began treating patients with advanced cancer, using a Kelley-based enzyme approach, with immediate good results. One of the first patients who consulted me had been diagnosed two years earlier, after a series of mishaps, with inflammatory breast cancer, the most aggressive form of the disease.

This patient had a very unfortunate story: by the time of her original diagnosis in 1985, her breast tumor was too large to allow for surgery, so her doctors recommended a course of radiation to the chest, hoping to shrink the tumor and allow for mastectomy.

She proceeded with the planned radiation, but at surgery the tumor was still quite large at 8 cm, with 18 of 18 lymph nodes involved with cancer.

Her doctors informed her that her disease would inevitably prove fatal, but suggested aggressive chemotherapy to hold off the cancer as long as possible. She again followed her doctor’s advice, beginning multi-agent chemo.

In the fall of 1987, two years into treatment, she developed evidence of new metastatic disease in the bone. At that point, she began looking into alternative approaches, learned about our work from a social worker she knew, and came under my care only a couple of months after I had begun in private practice.

To summarize her nearly 26 years of treatment with me, she has been disease-free for years as per bone scan studies, continues on her nutritional program, and continues leading a normal, cancer-free life.

By the standards of conventional oncology, this patient’s complete regression of metastatic disease and very long-term survival must be considered remarkable.

One of my favorite patients, whom I have discussed at times in my lectures, was diagnosed in August 1991 with stage IV pancreatic cancer, with multiple metastases into the liver, into the lung, into both adrenals, and into the bone. After a lung biopsy confirmed adenocarcinoma, his doctors discouraged chemotherapy, telling him and his wife conventional treatments would only ruin his quality of life while offering no benefit.

He was given, as he would later tell me, two months to live.

The patient’s wife, a former college professor with an interest in nutritional medicine, learned about our approach from an article she read in an alternative health journal, and in the fall of 1991 he began treatment with me. Some fifteen months later, repeat CT scans showed stabilization of disease. Since he felt fine at the time, following his program religiously, he decided against any further conventional testing until 1998, seven years after he had started with me, when a series of CT scans confirmed total resolution of his once extensive cancer.

This patient would eventually die at age 85 in 2006, 15 years after his diagnosis, from the residual effects of a serious automobile accident.

To put his case in perspective, I know of no similar case with documented stage IV pancreatic cancer that had spread at the time of diagnosis into multiple organs who survived 15 years after diagnosis with confirmed total resolution of his disease.

For both these patients, in the traditions of the Kelley system I prescribed a plant-based, high carb diet, including multiple servings of fruit, with its content of natural sugar, along with four glasses of carrot juice daily. By Seyfried’s hypothesis, both of these patients should have died quick, miserable deaths under my care.

Currently, after more than 25 years in practice, I am writing a two-volume set consisting of detailed case histories of our own patients, like the two mentioned above, to make the point that the therapy works in practice. For those diagnosed with poor-prognosis solid tumors, many now alive in excess of 10 years, I have prescribed a high carbohydrate diet, in total contradiction to what Dr. Seyfried proposes as the ideal anti-cancer approach.

Just this week as I write this, one of my newer patients, a wonderful, creative inventor and computer whiz from the Washington, DC area, came into my office for his regularly scheduled six month re-evaluation appointment. When he started with me in January 2010, three and a half years ago, he had been diagnosed with stage IV metastatic squamous cell carcinoma of the lung, with multiple tumors in both lungs and with evidence of metastases in his ribs. His local doctors in DC had explained he had terminal disease, for which chemotherapy would be useless.

His rib lesions were causing him so much misery his doctors did suggest a course of radiation for palliative pain control. However, he had learned about my work from a mutual friend who recommended he dispense with all conventional treatments and instead pursue my regimen.

He followed her advice, refused radiation, came to see me, and over the years he has proven to be a very vigilant, determined and compliant patient. Within a year on his nutritional program, which includes a high carb diet, his pain had resolved, his energy, stamina, and concentration had improved, and scans confirmed total resolution of all his original extensive disease – in complete contradiction to what Dr. Seyfried would predict or claim possible.

When I saw the patient in my office during this recent visit, he remarked that over the preceding months, he had been craving more carbs than ever before, so in response he had significantly increased his daily intake of carrot juice, fruits, and starchy vegetables, foods allowed on his diet with no limitation.

With this increased carb intake, he has actually lost 16 pounds of excess weight, and his energy is better than it has been in 30 years. And, he remains cancer free. According to Dr. Seyfried, on this high-carb regimen his cancer, thriving as he claims on sugars, should long ago have exploded with deadly results.

Despite Kelley’s and my own positive experience treating cancer patients with non-ketogenic, often high-carb diets, can I muster any data, past or present to support what Seyfried claims? What does past experience and current data show, about the miracle of the ketogenic diet for cancer?

In my previous articles, I discussed my friend, the late Dr. Robert Atkins, the famed diet doctor, who long before Dr. Seyfried appeared on the scene hoped his “ketogenic” diet might be an answer to cancer. During the late 1980s and right through most of the 1990s, Dr. Atkins treated hundreds of cancer patients, many, though not all, with a ketogenic diet, along with a variety of supplements and intravenous vitamin C.

It was 1992, when his chief IV nurse, who had been with him for years, called me, wishing to take me to lunch. I knew him through my friendship with Dr. Atkins, and in fact he had been quietly referring a number of patients to me from the clinic, patients who were not responding to the Atkins’ treatment.

We did meet for lunch several days later, and I was surprised that after some general chatter, he asked me point blank if there was any chance he could work for me! He seemed quite serious, but I explained that my colleague Dr. Linda Isaacs and I didn’t use IV treatments so I would have no use for his particular skills.

Now intrigued, I asked why he would want to change jobs, since our practice was by design slower paced, whereas Bob ran a very busy clinic and active IV unit which would seem perfectly suited for this nurse’s expertise. He then explained, with obvious disappointment, that none of the hundreds of cancer patients they had treated or had been treating had responded to any significant degree, with the exception of those he had referred to me.

The failures had taken an emotional toll on the nurse, who was ready for a change.

Though I would see Bob occasionally at conferences, I never mentioned any of this to him. Some years later we met for lunch in Washington, DC, at a conference where we were both scheduled to speak. To my astonishment, he told me he was closing down his cancer unit completely, to concentrate on his traditional area of expertise – obesity, diabetes, heart disease, hypoglycemia, the metabolic syndrome – problems for which he knew his nutritional approach with the ketogenic diet worked quite effectively.

In terms of cancer, after more than ten years of trying on hundreds of patients, his treatment had been a disappointment. I certainly appreciated his honesty, and was gratified when he expressed his admiration for what he had been hearing about my successes.

I think it was still hard for him to accept that many cancer patients, and many humans without cancer, did best on a plant-based, high carb diet, so foreign to his way of thinking. Though he had heard me expound on the Kelley approach many times over the years, it was to him implausible that humans as a species had adopted to a variety of diets, some high fat, some high carb, some more balanced, and that in medical practice, we as physicians had to be aware that different patients might require completely different diets for optimal health.

To his grave, as far as I know, he believed that all humans should be on a high fat diet with minimal carbs.

In my opinion, Bob Atkins knew more about the theory and practice of the ketogenic diet, its benefits and limitations, including as applied to cancer patients, than anyone in the history of medicine. For him, the concept was hardly the musings of a PhD laboratory scientist, but the practical observations of a physician who treated thousands of patients over decades. And for cancer, the ketogenic diet just did not seem to work.

Bob wasn’t the only physician, his clinic not the only place, where the ketogenic diet has been applied in modern times. At the Johns Hopkins Medical Center, for many years a group of researchers and neurologists have prescribed a very strict ketogenic diet for children with intractable seizures, that is, seizures unresponsive to currently available medications. For this particular indication, in adults as well as children, the diet works quite well.

So, what evidence does Dr. Seyfried himself provide to prove his point that the best diet for all cancer patients, whatever the type, is the ketogenic, high fat, no carb diet? Well, very little. Certainly the 400 plus pages of elaborate biochemistry and theory are impressive and informative. But in terms of practicalities, that is, results with actual human patients diagnosed with cancer, there is next to no evidence.

Dr. Seyfried does include a chapter toward the book’s end entitled “Case Studies and Personal Experiences in using the Ketogenic Diet for Cancer Management.” Here, Dr. Seyfried provides a description of a pilot study, written by the investigators themselves, discussing the use of the ketogenic diet in children with inoperable brain cancer. However, the authors admit the study was intended only to evaluate the diet’s tolerability and effect on glucose metabolism as determined by PET scanning, not treatment benefit or survival.

As the authors write, “the protocol was not designed to reverse tumor growth or treat specific types of cancer.” The researchers also acknowledge the patient numbers were too small to allow for meaningful statistical evaluation, even for the avowed purposes. Overall, the discussion centers on the practicalities of implementing the diet and the results of the PET scans.

Interesting information, but hardly useful in terms of treatment effect.

In this same chapter, there are also two case reports, neither very impressive. The first, written by the mother, tells the story of a four-year old child diagnosed in 2004 with a low-grade (less aggressive) but quite large and inoperable brain tumor. The parents, as the mother writes, entrusted their child into the hands of the experts, who prescribed the usual “gold standard” treatments, which are not clearly described initially but presumably mean chemotherapy and perhaps radiation.

In subsequent years, the boy continued on aggressive conventional therapeutics, when in 2007, the parents learned of the preliminary research of Dr. Seyfried. While continuing low-dose chemotherapy combined with the ketogenic diet, the patient experienced a “15%” reduction in tumor size. The chemo was eventually discontinued while the parents maintained their son on the ketogenic diet, and the child, sadly, eventually died.

In my monograph One Man Alone, I included a case report of a patient treated by Kelley, diagnosed with an inoperable and very aggressive form of brain cancer that had spread into the spinal canal. After failing radiation, the patient began treatment with Dr. Kelley in 1981. At the time, the patient’s wife actually had to administer the treatment, even the coffee enemas, since the patient himself was largely incoherent and wheelchair bound.

As I wrote in my book, “Nevertheless on the therapy [Kelley’s] he slowly began to improve, to the point his mental status normalized and over a period of a year, he progressed from a wheelchair to a walker to a cane.” When I completed my study in 1987, he had survived 5 years and was in excellent health, with no evidence of cancer in his brain or spinal canal.

A second brief report in Seyfried’s “Case Studies” chapter, this time written by the patient himself, describes a physician who had been diagnosed in 2009 with multiple myeloma, a cancer affecting the bone and bone marrow. The diagnosis came about when the physician fractured his arm while lifting weights.

After scouring the literature, he became quite attracted to the “good science” behind the ketogenic hypothesis, so under Dr. Seyfried’s direct supervision, he began the diet. Though the patient seems quite enthusiastic about his response, he admits in his note that with the diet there has been “no progression,” presumably in terms of x-ray studies, and some improvement in the blood studies. He still considers his disease as “incurable.”

First of all, myeloma patients, even when diagnosed with an aggressive form, often linger for years before the disease advances. I would never have included such a two-year survivor in One Man Alone, or in any other book I have written or plan to write – unless, possibly, there has been documented significant regression of disease, not apparent in this case. I do include a case of multiple myeloma treated by Dr. Kelley in my monograph, a woman diagnosed with extensive cancer throughout her skeleton with evidence of multiple fractures.

When she first consulted with Dr. Kelley in 1977 she was in a near terminal state after having failed intensive chemotherapy. Nonetheless, despite her dire situation within a year she had experienced complete regression of her extensive bony lesions, as documented by x-ray studies. Though in subsequent years her compliance with her nutritional regimen would waver and her disease would in turn recur, invariably when she resumed Kelley’s treatment the myeloma would go into remission.

At the time I finished the monograph in 1987, she had survived 11 years. I found this case acceptable for my Kelley report, but a two-year survivor with no evidence of disease regression but lots of enthusiasm, I would never had included.

I might add that for myeloma patients, Dr. Kelley prescribed, and I prescribe, a high fat diet – but never ketogenic.

Why, one wonders, if Dr. Seyfried’s actual data is so thin, have so many physicians, scientists, and writers jumped on the ketogenic bandwagon?

Let me say out front I have no problem with scientists who propose a theory, in short papers or in the case of Dr. Seyfried, in long, detailed books. I do have a problem when scientists go a step further, insisting in the absence of any significant human data or even impressive case histories they have unraveled the mystery of cancer. I am also quite surprised, in the case of Dr. Seyfried, that both alternative and conventional practitioners have risen up in a loud chorus of enthusiasm, as if indeed Dr. Seyfried’s theories are correct, and that he has solved the cancer riddle.

I found a typical response to Seyfried’s book in a review on Amazon, written by the esteemed conventional oncologist Dr. Stephen Strum:

I am a board-certified medical oncologist with 30 years experience in caring for cancer patients and another 20 years of research in cancer medicine dating back to 1963. Seyfried’s “Cancer as a Metabolic Disease” is the most significant book I have read in my 50 years in this field. It should be required reading of all cancer specialists, physicians in general, scientific researchers in the field of cancer and for medical students. I cannot overstate what a valuable contribution Thomas Seyfried has made in writing this masterpiece.

From the alternative front, on his website read literally by millions, Dr. Joseph Mercola has been an enthusiastic supporter of Dr. Seyfried and his ketogenic thesis. In two lengthy articles Dr. Mercola proposes that the ketogenic is an answer to cancer.

In the first posting appearing on his site June 16, 2013, based on an interview with Dr. Seyfried, Dr. Mercola writes in his introductory paragraph:

Could a ketogenic diet eventually be a “standard of care” drug-free treatment for cancer? Personally, I believe it’s absolutely crucial, for whatever type of cancer you’re trying to address, and hopefully someday it will be adopted as a first line of treatment.

In a second article from June 30, 2013, entitled “The Ketogenic Diet – An Excellent Approach to Cancer Prevention and Treatment,” Dr. Mercola discusses the work of Dr. Dominic D’Agostino, PhD, another basic scientist, this time from Florida, who enthusiastically reports his animal and laboratory work with the ketogenic diet.

As I ponder this enthusiasm, I have to think that perhaps I am just a little slower, or more cautious, than most. The day after I first met Dr. Kelley in New York in July 1981, I was on a plane to Dallas to begin my review of Kelley’s charts. As previously discussed, I quickly found among Kelley’s records case after case of appropriately diagnosed poor-prognosis and/or terminal cancer, patients alive five, ten, even 15 years later, with no possible explanation for such survival other than Kelley’s odd nutritional treatment.

After I returned to New York some three weeks later carrying with me copies of dozens of patient records, and after reviewing my findings with Dr. Good, I knew Kelley was on to something. One thing for sure, at the time I didn’t, as I easily could have with my journalism contacts, think about “explosive” news stories, or a book contract.

Quite the contrary, as I discussed in a previous article, I met Kelley through a journalist friend who thought he might make an excellent subject for a potboiler, a wealth-generating best seller. After only a few days in Kelley’s Dallas office, I quickly realized that he, as odd as he may have seemed to some, as peculiar as his therapy might be to conventional researchers, had put together a potentially useful, non-toxic, nutritional cancer treatment.

I also quickly understood that for his approach to gain academic acceptance, Kelley must back off completely from involvement with popular controversial books and media hysteria. When I expressed my opinion about such things to him, he accepted the wisdom of my position unconditionally. When he then told my writer friend in a rather difficult phone call that he had no interest in pursuing the book she had suggested, she was, to say the least, livid with me – especially since she had brought Kelley and me together in the first place, seeking my opinion about his authenticity.

Ironically, because I thought him to be possibly legitimate, I had instructed him to avoid involvement with any popular book including hers. My writer friend would not speak to me for 16 years, until we met at a conference in New York. We hugged, after all those years, and made up.

Only after interviewing 1,000 of Dr. Kelley’s patients, and evaluating 455 of them at length over a five-year period, did I even begin to think about the book that would be written – not a popular potboiler, not a tome expounding his elaborate theories, but a serious academic monograph about our findings. It is just not in my makeup to put out a book with lovely theory and two case reports, however inspiring they might be.

I do have a challenge, a gentlemanly academic challenge of course, to Dr. Seyfried.
In this article, I have presented a number of cases, seven to be exact, four from Kelley’s files and three from my own practice. The four Kelley cases include the 31-year survivor of metastatic pancreatic cancer confirmed at Mayo, the 34-year survivor of stage IV endometrial cancer, the five-year survivor of aggressive brain cancer, and the 11-year survivor of advanced, aggressive multiple myeloma.

The three from my practice include the stage IV 25-year survivor of metastatic inflammatory breast cancer, my 15 year survivor of stage IV pancreatic cancer, and my three and a half year survivor of stage IV lung cancer that has totally regressed on my therapy.

With the exception of the myeloma patient, all the other six patients, both Kelley’s and mine, followed a high carb, plant-based diet, replete with frequent servings of fruit and multiple glasses daily of sugar-rich carrot juice. I challenge, for the benefit of science, Dr. Seyfried to match these seven simple straightforward cases. In my experience, no one else has been able to meet the challenge, so I question whether Dr. Seyfried can either.

The point I’m trying to make is simple.

  • In science, as in most walks of life, a little caution certainly goes a long way.
  • Within my practice, I am already receiving letters and faxes and calls from prospective patients diagnosed with advanced cancer of a variety of types, who with great enthusiasm jumped on the ketogenic diet bandwagon – with poor results.

In my next and final article in this series on the ketogenic diet as a cancer treatment, I will offer my suggestions as to why the diet most likely won’t work for most people, based on past epidemiological research and current biochemical thinking.

First, as Weston Price proved 70 years ago in his exhaustive epidemiological study, over the millennia different groups of humans adjusted to different types of diets, depending on the locale in which they lived and the available food therein, ranging from high carb to virtual no carb. Though Dr. Price was not evaluating dietary treatments as such for disease, his point should nonetheless be well taken – different humans (for optimal health) need different diets.

In terms of our specific discussion, diet as cancer treatment, Dr. Kelley demonstrated more recently in his Dallas, Texas, and Winthrop, Washington offices, no one diet suits all patients diagnosed with the disease, quite the contrary. Over a 20 year period working in the trenches treating many thousands of people, Dr. Kelley came to learn that each patient who walked into his office required a diet designed specifically for his or her metabolic needs, and these dietary requirements could vary enormously from patient to patient.

Unknown to most, even within the alternative world, my friend Bob Atkins tried the ketogenic diet for some 12 years on many of his cancer patients, with no significant success as he reported to me. As a telling point, under the name “Dr. Robert Atkins” on Amazon, one will find dozens of books he authored including his original diet book, its many incarnations and editions, along with books on vitamins, minerals – but glaringly absent, no book on cancer. Yes, the ketogenic diet has been tried before, with cancer patients, and without success.

I also might offer a thought as to why, from a more esoteric, more biochemical perspective, for most people diagnosed with cancer the ketogenic diet might not work. For the past 150 years, researchers have approached cancer as a disease in which perfectly happy, normal mature cells sitting in some tissue somewhere suddenly go awry, lose their normal regulatory restraint, develop a primitive, undifferentiated appearance or phenotype, begin proliferating without restraint, begin invading through tissues and organs, begin migrating, spreading, creating new blood vessels along the way to feed the rapacious appetite of cancer. But over the past 15 years, gradually, a new, more productive, and I believe more truthful hypothesis has emerged, spearheaded particularly by Dr. Max Wicha at the University of Michigan. Scientists such as Dr. Wicha have discovered that cancer may be a little more complicated than we have thought these long decades.

In recent years stem cells have been a hot topic in the research world, and a hot topic, for better or worse, in the media. These headline-grabbing stem cells are primitive undifferentiated cells, located as nests in every tissue and organ in the body, that serve as a reserve supply to replace cells in the tissue or organ lost due to normal turnover (as in the bone marrow or along the intestinal lining), disease, injury, or cell death.

In this way, stem cells allow complex life to exist and continue, providing tissue replacements as needed, appropriate for the tissue in which they live. That is, liver stem cells will create new liver cells as needed, bone marrow stem cells will create new bone marrow clones as required, intestinal stem cells will form, as necessary, intestinal lining cells. In this way, the developmental capacity of stem cells seems to be governed by the local environment.

After stem cells were discovered in the 1960s, scientists initially thought that they had a limited repertoire, that is, liver stem cells can only create more liver cells, but not bone marrow or intestinal cells, bone marrow stem cells can only create more bone marrow cells, but not liver cells, and so on. But we now know that isn’t the case.

Stem cells, wherever they may be found, can adapt quite nicely, and are far more flexible than originally believed. In laboratory animals, a liver stem cell placed into the bone marrow starts creating not liver, but bone marrow cells, a bone marrow stem cell transplanted into the liver begins to generate not bone marrow, but liver cells. The environment appears to be the key, ultimately determining the direction of stem cell development.

In terms of cancer specifically, many scientists believe that the disease does not develop from normal healthy cells that for some reason go molecularly berserk, but from stem cells that have lost their normal regulatory controls, creating in turn the disease we know as cancer.

Like any normal tissue or organ, in a tumor these cancer stem cells generate a variety of cell types that can mature to some extent, but the stem cells remain always primitive, undifferentiated, capable of replicating endlessly, capable of killing eventually. Most standard therapies fail, Dr. Wicha and his associates believe, because they attack the more mature tumor line, not the essential tumor stem cells, the actual engines of cancer creation.

Dr. Seyfried makes the case that normal stem cells, like cancer cells, are obligatory glucose consumers, relying solely on anaerobic glycolysis for the energy needed for survival. I agree, to a point. But I will also make the case that as with normal stem cells, cancer stem cells are very flexible, capable of adjusting to the local environment.

If deprived of oxygen, stem cells happily will turn to glycolysis as the main source of ATP energy. In an oxygen rich environment, I believe these stem cells can adapt accordingly, recoupling at least to some extent glycolysis to the citric acid cycle and electron transport, with great efficiency, and in terms of cancer, with deadly results.

Some years ago, a patient of mine, a professor at a well-known university, became interested in oxygenation therapies for cancer, used widely in the Mexican Clinics. These “oxygen” treatments were an offshoot of Dr. Warburg’s work, i.e., that cancer cells as obligatory anaerobes can synthesize needed energy supplies only via glycolysis. Therefore, the theory goes, in the presence of oxygen, particularly ozone, a form of hyped up oxygen, cancers cells, unlike normal cells, will be poisoned.

My professor patient seemed quite taken by the ozone approach, which he thought I should start implementing in my practice. However, I become somewhat doubtful about the theory, and the use of ozone as a treatment for cancer. At the time I had already taken care of dozens of patients who prior to consulting with me had been to the Mexican Clinics to receive ozone along with other treatments.

All seemed to have initial good responses followed by explosive return of their malignancy. I explained to my professor patient that I believed cancer stem cells could quickly adapt to oxygen, despite what the Warburgians might claim.

At about this time, ironically, this professor’s dog developed a very aggressive sarcoma, for which standard treatments were of no avail. Enchanted by oxygenation therapies, he actually bought an ozone generating machine meant for rectal installation, which he began, against my advice, using on his most patient dog.

After two weeks, the large tumors, quite evident to the naked eye, regressed substantially, to the professor’s great joy. He called me with the good news, and in a collegial sense, suggested he might be teaching me, the cancer expert, something new. I told him to wait before we came to a conclusion.

Unfortunately, some four weeks later, the professor called me again, reporting sadly that after the initial miraculous response, the tumors had recurred with a vengeance, and the dog had quickly succumbed.

It’s an interesting story but of course just that, a story that I fully acknowledge proves nothing, though in my mind it does illustrate how adaptable cancer cells, specifically cancer stem cells can be. It is a good lesson, for all of us, before we tout the next great cancer miracle.

This article originally appeared on Natural Health 365.

Chris Beat Cancer: A Comprehensive Plan for Healing Naturally, published by Hay House, is a National Bestseller as ranked by USA Today, The Wall Street Journal, and Publishers Weekly! Get it on Amazon here, or anywhere books are sold.

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EAT-Lancet's Plant-Based Planet: 10 Things You Need to Know

An important new study about global nutrition was published this week that deserves everyone’s full attention: "Food in the Anthropocene: the EAT-Lancet Commission on healthy diets from sustainable food systems." [Don’t let the title intimidate you: You need to know what’s inside.] This paper was commissioned and published by The Lancet — one of the world’s oldest and most respected medical journals — and penned by an international group of 37 scientists led by Dr. Walter Willett of Harvard University.

The product of three years of deliberation, this 47-page document envisions a “Great Food Transformation” which seeks to achieve an environmentally sustainable and optimally healthy diet for the world’s people by 2050. Its core recommendation is to minimize consumption of animal foods as much as possible, and replace them with whole grains, legumes, and nuts.

We all want to be healthy, and we need a sustainable way to feed ourselves without destroying our environment. The well-being of our planet and its people are clearly in jeopardy, therefore clear, science-based, responsible guidance about how we should move forward together is most welcome.

Unfortunately, we are going to have to look elsewhere for solutions, because the report fails to provide us with the clarity, transparency and responsible representation of the facts we need to place our trust in its authors. Instead, the Commission’s arguments are vague, inconsistent, unscientific, and downplay the serious risks to life and health posed by vegan diets.

1. Nutrition epidemiology = mythology

The vast majority of human nutrition research — including the lion share of the research cited in the EAT-Lancet report — is conducted using the tragically flawed methodology of nutrition epidemiology. Nutrition epidemiology studies are not scientific experiments they are wildly inaccurate, questionnaire-based guesses (hypotheses) about the possible connections between foods and diseases. This approach has been widely criticized as scientifically invalid [see here and here], yet continues to be used by influential researchers at prestigious institutions, most notably Dr. Walter Willett. An epidemiologist himself, he wrote an authoritative textbook on the subject and has conducted countless such studies, including a recent, widely-publicized paper tying low-carbohydrate diets to early death. In my reaction to that study, I explain in plain English why epidemiological techniques are so untrustworthy and include a sample from an actual food questionnaire for your amusement.

Even if you think epidemiological methods are sound, at best they can only generate hypotheses that then need to be tested in clinical trials. Instead, these hypotheses are often prematurely trumpeted to the public as implicit fact in the form of media headlines, dietary guidelines, and well-placed commission reports like this one. Tragically, more than 80% of these guesses are later proved wrong in clinical trials. With a failure rate this high, nutrition epidemiologists would be better off flipping a coin to decide which foods cause human disease. The Commission relies heavily on this methodology, which helps to explain why its recommendations often fly in the face of biological reality.

2. Red meat causes heart disease, diabetes, cancer. and spontaneous combustion

The section of the report dedicated to protein blames red meat for heart disease, stroke, type 2 diabetes, obesity, cancer, and early death. It contains 16 references, and every single one is an epidemiological study. The World Health Organization report tying red meat to colon cancer was also mentioned, and that report is almost entirely based on epidemiology as well. [Read my full analysis of the WHO report here.] The truth is that there is no human clinical trial evidence tying red meat to any health problem. I certainly haven’t found any — and if there were, I think this Commission surely would have mentioned it.

Yet even in this “red meat is an apocalypse on a plate” section, meat’s virtues peek through:

[In sub-Saharan Africa] . growing children often do not obtain adequate quantities of nutrients from plant source foods alone…promotion of animal source foods for children, including livestock products, can improve dietary quality, micronutrient intake, nutrient status, and overall health.” [page 10]

3. Protein is essential… but cancerous

“Protein quality (defined by effect on growth rate) reflects the amino acid composition of the food source, and animal sources of protein are of higher quality than most plant sources. High-quality protein is particularly important for growth of infants and young children, and possibly in older people losing muscle mass in later life.” [page 8]

Translation: Complete proteins are good because they contain every essential amino acid. All animal proteins are naturally complete, whereas most plant proteins are incomplete. Watch how the authors wriggle their way out of this inconvenient truth in the next sentence:

“However, a mix of amino acids that maximally stimulate cell replication and growth might not be optimal throughout most of adult life because rapid cell replication can increase cancer risk.” [page 8]

Translation: Complete proteins are bad because they cause cancer.

The sole reference for this absurd suggestion that complete proteins cause cancer is a paper about mutations causing cancer in which the terms “protein,” “amino acid,” and “meat” each occur a grand total of zero times, suggesting that the Commission’s suggestion is pure. suggestion. Furthermore, if obtaining all of the essential amino acids we need causes cancer, shouldn't we also worry about complete proteins from plant sources like tofu or beans with rice?

4. Omega-3s are essential. good luck with that

“Fish has a high content of omega-3 fatty acids, which have many essential roles… Plant sources of alpha-linolenic acid [ALA] can provide an alternative to omega-3 fatty acids, but the quantity required is not clear.” [page 11]

If the Commission doesn’t know how much plant ALA a person needs to consume to meet requirements, then how does it know that plants provide a viable alternative to omega-3s from animal sources?

The elephant in the room here is that all omega-3s are not created equal. Only animal foods (and algae, which is neither a plant nor an animal) contain the forms of omega-3s our bodies use: EPA and DHA. Plants only contain ALA, which is extremely difficult for our cells to convert into EPA and DHA. According to this 2018 review, we transform anywhere between 0% and 9% of the ALA we consume into the DHA our cells require.

Instead of being vague, why not responsibly warn people that trying to obtain omega-3 fatty acids from plants alone may place their health at risk?

“About 28 g/day (1 ounce) of fish can provide essential omega-3 fatty acids… therefore we have used this intake for the reference diet. We also suggest a range of 0 – 100 g/day because high intakes are associated with excellent health.” [page 11]

Wait… if it takes 28 grams to meet your daily requirement for omega-3s AND high intakes are associated with excellent health, why allow the range to begin at ZERO grams per day? If the Commission doesn’t feel comfortable recommending fish, it should at least recommend algae-sourced omega-3 supplements.

5. Vitamins and minerals are essential… so take supplements

The drumbeat heard throughout the report is that animal foods are dangerous and that a vegan diet is the holy grail of health, yet EAT-Lancet commissioners repeatedly find themselves in the awkward position of having to acknowledge the nutritional superiority of the very animal foods they recommend avoiding:

"Although inclusion of some animal source foods in maternal diets is widely considered important for optimal fetal growth and increased iron requirement, especially during the third trimester of pregnancy, evidence suggests that balanced vegetarian diets can support healthy fetal development, with the caveat that strict vegan diets require supplements of vitamin B12." [page 13]

“Adolescent girls are at risk of iron deficiency because of rapid growth combined with menstrual losses. Menstrual losses have sometimes been a rationale for increased consumption of red meat, but multivitamin or multimineral preparation provide an alternative that is less expensive and without the adverse consequences of high red meat intake.” [page 13]

If the commissioners are concerned that red meat is dangerous (which is only true on Planet Epidemiology), why not recommend other naturally iron-rich animal foods such as duck, oysters, or chicken liver for these growing young women, as these foods would also provide the complete proteins needed for growth? What about the 10-22% of non-teen reproductive-age women in the U.S. who suffer from iron deficiency? And why a “multimineral preparation” rather than a simple iron supplement? Are they implying that other minerals may be lacking in their plant-based diet?

In changing to the EAT-Lancet diet, the Commission claims:

“The adequacy of most micronutrients increases, including several essential ones, such as iron, zinc, folate, and vitamin A, as well as calcium intake in low-income countries. The only exception is vitamin B12 that is low in animal-based diets [I believe this was an error on their part, since B12 is only found in animal foods.] Supplementation or fortification with vitamin B12 (and possibly with riboflavin [vitamin B2]) might be necessary in some circumstances.” [page 14]

Unfortunately, the nutritional inadequacy of plant-based diets goes beyond B vitamins. Plant foods lack several key nutrients, and some of the nutrients they do contain come in less bioavailable forms. Furthermore, many plant foods contain “anti-nutrients” that interfere with nutrient absorption. This means that just because a plant food contains a nutrient doesn’t mean we can access it.

An important example is that grains, beans, nuts, and seeds — the staple foods of plant-based diets — contain phytate, a mineral magnet which substantially interferes with absorption of essential minerals like zinc, calcium, iron, and magnesium. And thanks to oxalates — mineral-binding compounds found in a wide variety of plant foods — virtually none of the iron in spinach makes it into Popeye’s muscles.

Only animal foods contain every nutrient we need in its proper, most accessible form. To learn more about nutrient availability and how it affects brain health, read this article.

6. Making up numbers is fun and easy

How did the commissioners arrive at the recommended quantities of foods we should eat per day… 7 grams of this, 31 grams of that? Numbers like these imply that something’s been precisely measured, but in many cases, it’s plain that they simply pulled a number out of thin air:

“Since consumption of poultry has been associated with better health outcomes than has red meat, we have concluded that the optimum consumption of poultry is 0 g/day to about 58 g/day and have used a midpoint of 29 g/day for the reference.” [page 10]

Nowhere do they say that poultry is associated with any negative health outcomes, so why limit it to a maximum of 58 grams (2 ounces) per day?

The commissioners attempt to defend themselves from criticism on this issue by stating:

“We have a high level of scientific certainty about the overall direction and magnitude of associations described in this Commission, although considerable uncertainty exists around detailed quantifications.” [page 7]

If they are this uncertain about the details, how can they in good conscience prescribe such specific quantities of food? Why not say they don’t know? Most people will not read this report — they will interpret the values in this table as medical advice.

7. Epidemiology is gospel… unless we don’t like the results

Any researcher will tell you that clinical trials — actual scientific experiments — are considered a much higher level of evidence than epidemiological studies, yet Willett’s group not only relies heavily on epidemiological studies, it favors them over clinical trials when it suits their agenda:

“in large prospective [epidemiological] studies, high consumption of eggs, up to one a day, has not been associated with increased risk of heart disease, except in people with diabetes.

“However, in low-income countries, replacing calories from a staple starchy food with an egg can substantially improve the nutritional quality of a child’s diet and reduce stunting. [randomized clinical trial]

“We have used an intake of eggs at about 13 g/day, or about 1.5 eggs per week, for the reference diet, but higher intake might be beneficial for low-income populations with poor dietary quality.” [page 11]

Why recommend only 1.5 eggs per week when epidemiological studies found that 1 egg per day was perfectly fine? And why skew your recommendations against low-income people, who make up a significant portion of the global population?

There is a remarkable paragraph on page 9 (too long to quote here) arguing that red meat was found to increase the risk of death in epidemiological studies conducted in Europe and the USA, but not in Asia, where red meat (mainly pork) was associated with a decreased risk of death. Rather than grappling with this seeming contradiction, the Commission simply dismisses the Asian findings as invalid, wondering if perhaps Asian countries haven’t been rich long enough for the risk to show up yet.

8. Everyone should eat a vegan diet, except for most people

Although their diet plan is intended for all “generally healthy individuals aged two years and older,” the authors admit it falls short of providing proper nutrition for growing children, adolescent girls, pregnant women, aging adults, the malnourished, and the impoverished — and that even those not within these special categories will need to take supplements to meet their basic requirements.

Sadder still is the fact that the majority of people in this country and in many other countries around the world are no longer metabolically healthy, and this high-carbohydrate plan doesn’t take them into consideration.

"In controlled feeding studies, high carbohydrate intake increases blood triglyceride concentrations, reduces HDL [aka “good”] cholesterol concentration, and increases blood pressure, especially in people with insulin resistance.” [page 12]

For those of us with insulin resistance (aka “pre-diabetes”) whose insulin levels tend to run too high, the Commission’s high-carbohydrate diet — based on up to 60% of calories from whole grains, in addition to fruits and starchy vegetables — is potentially dangerous. The Commission half-acknowledges this by recommending that even healthy people limit consumption of starchy roots like potatoes and cassava flour due to their high glycemic index, but oddly does not mention grain and legume flours, or high glycemic index fruits, leaving the door open for processed food companies to market products like pasta, cereal and juice beverages to its plant-based planet. High insulin levels strongly increase the risk for numerous chronic diseases and can mean a lifetime of medications, disability, and early death. If the Commission read its own report it would find support for the notion that those of us with metabolic damage may be better off increasing our meat intake and decreasing our carbohydrate intake:

“In a large controlled feeding trial, replacing carbohydrate isocalorically with protein reduced blood pressure and blood lipid concentrations.” [page 8]

This was the 2005 OmniHeart trial, which used 50% plant protein and 50% animal protein. It would seem the only people who should eat a vegan diet are people who make the informed choice to eat a vegan diet, despite the risks.

9. Pay no attention to the money behind the curtain

As an advocate of meat-inclusive diets, I have often been assumed to have financial ties to the meat industry (which I do not), but how many people stop to question the financial (and professional) incentives that may influence doctors promoting plant-based diets? We all have personal beliefs and we all need to make a living, but honesty with oneself and transparency with the public should be paramount. The Nutrition Coalition has compiled a list of Dr. Willett's potential conflicts of interest here.

The EAT Foundation, which collaborated with The Lancet to produce this report, was founded by Norwegian billionaire and animal rights activist Gunhild Stordalen. EAT recently helped to launch "FReSH" (Food Reform for Sustainability and Health), a global partnership of about 40 corporations, including Barilla (pasta), Unilever (meat alternatives and vegetable oils), Kellogg's (cereals) and Pepsico (sugary beverages). Make of this what you will.

10. No to choices, yes to taxes?

How does EAT-Lancet propose to achieve its dream of a plant-based world? Many suggestions are put forth, but two are worth emphasizing: the elimination or restriction of consumer choices, and taxation. The EAT Foundation describes itself as:

"a non-profit startup dedicated to transforming our global food system through sound science, impatient disruption and novel partnerships.”

Sound science? Clearly not. But impatient disruption — what does that mean?

Regardless of how you feel about taxation as a tool for social change, consider the Commission’s own numerous exceptions to the plant-based rules, including pregnant women, children, the malnourished and the impoverished. Should we really support making animal foods — the only nutritionally complete foods on Earth — even more expensive for vulnerable populations? The notion of taxation is followed by a vague reference to the possibility of “cash transfer” social safety nets for women and children. This section of the report is representative of its overall elitist and paternalistic tone.

I believe, because I’m convinced by the science, that animal foods are essential to optimal human health. This is an uncomfortable biological reality we all have to wrestle with as creatures of conscience. Finding ways to support excellent health and quality of life for the creatures we depend on for our sustenance and vitality is one of our most important callings as caring stewards of our planet and all of its inhabitants. But I’m also a firm believer in personal choice. We each need to become experts in what works best for our own bodies. Eat and let eat, I say. It seems clear that EAT-Lancet commissioners are neither supporters of personal choice nor the transparent distribution of accurate nutrition information that would empower people to weigh the risks and benefits of various diets for themselves.

Challenge Authority

The EAT-Lancet report has the feel of a royal decree, operating under the guise of good intentions, seeking to impose its benevolent will on all subjects of planet Earth. It is well worth challenging the presumed authority of this group of 37 “experts,” because it wields tremendous power and influence, has access to billions of dollars, and is likely to affect your health, your choices, and your checkbook in the near future.

Capitalizing on our current public health and environmental crises, the EAT-Lancet Commission pronounces itself as the authority on the science of nutrition, exploits our worst fears, and seeks to dictate our food choices in accordance with its members' personal, professional and possible commercial interests.

To the best of my knowledge, there has never been a human clinical trial designed to test the health effects of simply removing animal foods from the diet, without making any other diet or lifestyle changes such as eliminating refined carbohydrates and other processed foods. Unless and until such research is conducted demonstrating clear benefits to this strategy, the assertion that human beings would be healthier without animal foods remains an untested hypothesis with clear risks to human life and health. Prescribing plant-based diets to the planet without including straightforward warnings of these risks and offering clear guidance as to how to minimize them is scientifically irresponsible and medically unethical, and therefore should not form the basis of public health recommendations.

Watch the video: ΣΩΜΑ Σκελετός ΝΗΠΙΑΓΩΓΕΙΟ- ΔΗΜΟΤΙΚΟ (June 2022).