Nutritional Ketosis is an Oxymoron II: The Last Ketotic Gasp

gratuitous image of
the Drs. Eades, early 2015
A little while back I wrote Nutritional Ketosis is an Oxymoron.  I was taken to task a bit in comments for the inappropriate use of oxymoron, but I'm going to plead for leniency in the spirit of the use of the term.  The crux of that post was that the terms nutritional (as in being in a calorically sufficient, weight stable state) and ketosis are metabolically contradictory.  This is perhaps evidenced in no more profound manner than the extremes required to produce and sustain such a state, and the ease with which it is abolished.

Ketowars rage on as the standard bearer appears to be imploding on the sidelines ...  I got into a discussion on Twitter with Dr. Eades about a side issue, and here you go ...


  1. Starvation ketosis is distinctly different from nutritional ketosis.
  2. No human populations in sustained nutritional ketosis (not even the Inuit).
  3. Dietary reasons why the Inuit weren't in nutritional ketosis
  4. Genetic reasons why the Inuit weren't in nutritional ketosis
  5. Ketosis doesn't really matter, the Inuit were fat burning beasts.
  6. Vilhjalmur Stefannson ate like an Inuit for a year and he was healthy.
  7. No long term RCTs for VLC or ketogenic diets
  8. Lack of evidence for "nutritional ketosis" in short-term RCTs
  9. Keto for Epilepsy
  10. NuttyK vs. True Keto:  A Two-Way Context Problem

If you wish to skip to any section, you can C&P part or all of any of the phrases above into your browser's search function.

1. Starvation ketosis is distinctly different from nutritional ketosis.

Humankind has historically gone through periods of short term and long term starvation and thus ketosis.  This may well have had a long term protective effect on overall health and longevity, countering periods of relative excess.  The literature is full of populations living in four season environments, going to great lengths to avoid annual starvation in late winter and early spring, and those further north being virtually unable to avoid it entirely.  Then there would be longer term climate trends that caused lengthy famines.

Under these conditions, ketosis is a metabolic adaptation to minimize the damage of a chronic catabolic state.  This doesn't mean that ketosis is damaging in and of itself.  But, one has to wonder why, if our metabolisms are clearly capable of sustaining ketosis, we don't just run on ketones all the time if such a metabolic state is in any way "favorable" or "advantaged".   In a time of scarcity of exogenous fuel, one can envision that a less well regulated metabolism can be put into place ... even allowed to run full stop.   Ketones bypass certain regulatory mechanisms and in certain illnesses this provides a therapeutic benefit.

2. No human populations in sustained nutritional ketosis (not even the Inuit).

This is really the bottom line here, which got me into an inadvertent Twitter tussle with LC Scam Wow guy Dr. Mike Eades.   This turned quickly to him trying to turn the tables on me, requiring me to prove they are not in ketosis.   But here's the thing.  It is Dr. Eades and his ilk who are making extraordinary claims vis a vis the healthfulness of what I call NuttyK.  Thus it is Dr. Eades and his ilk who bear the burden of proof.  Just as the vegan proponents bear the burden of proof that animal-food-free diets are healthy for the long term.  People can do all the n=1s for a year or few, or clinical trials with unknown adherence for a few months to two years ... these still don't really tell us about long term effects.

Hate him all you want, but Ancel Keys looked to see what it was about the diets of countries with low heart disease rates had in common, and/or  where they differed from the diet in the US and other countries with higher CVD rates.  Similarly, Weston Price and Dan Beuttner looked for dietary patterns associated with health and longevity.  The paleo and other IHC folks love to cite various studies of the Masai and the Inuit, and various other cultures that ostensibly consumed a high fat diet.   However, the vast majority of peoples around the globe were consuming enough carb to not be in ketosis in the fed state, pretty much ever.  There are very few that would qualify as low carbohydrate diets, so the "poster cultures" for your basic LC or VLC culture are pretty rare even for that.  I've done a number of posts over the past couple of years regarding what many of these cultures actually ate.  It only gets worse as one after another, we learn things weren't quite as extreme as portrayed, or worse, almost the opposite.

almost definitely NOT
in "nutritional ketosis"

Which leaves us pretty much with a single general population (arctic dwelling humans), of which the Inuit have been involuntarily designated to represent.   Again, onus is on the Eades ilk to support their assertions about this population, not the other way around.   I'm not going to rehash this with links, because frankly I just don't have the time.  Feel free to post links in comments to studies like Heinbecker, etc., or even to the various Duck Dodgers posts on the topic over on FTA.   

The metabolic assessments of actual Inuit have failed to show ketosis.

3.  Dietary reasons why the Inuit weren't in nutritional ketosis:

There are several reasons why the Inuit do not manifest "nutritional ketosis":
  • Diet is High Protein and High Fat (but not so high):  The Inuit diet averages out to be roughly 55% fat and 45% protein, not the 70, 80, even 90% fat I've seen claimed.  It is virtually impossible to get above 60% fat on a whole foods diet, and you'd really need plants (e.g. avocados, olives, coconut) because with animals, eating fat in meat and organs and marrow of animals (even cold water dwellers) isn't going to get you there.  
Before continuing, the above is likely the number one dietary reason why they are not in ketosis.   At over 250g protein/day, there is a large excess of protein  (excess to what is required to maintain muscle, etc.) that would be deaminated and fed into Krebs for energy production.  This would keep Krebs "churning".  To this we can add:
  • Carb Intake May Be Underestimated:  The amount of carb ingested may be higher than generally reported.  Sea mammals in particular have higher glycogen content, including glycogen in adipose tissue which is normally ignored in most animals.   
  • Lactic Acid = "Carb":  Glycogen may break down to lactic acid, but this is also considered to be a "carbohydrate" fuel.
  • Odd Chain Fatty Acids:  Fat in sea mammals is not-insignificant in odd chain fatty acids (OCFA).  When these are oxidized, you're left with a 3-carbon fragment at the end (proprionate) that is a substrate for gluconeogenesis.  Dietary  OCFA would incorporate into adipose tissue and be oxidized in fasting.  Hard to tell if it would be significant compared to some animal studies, but OCFA metabolism has been shown to elevate glucose production and decrease ketogenesis.
  • Fermented Protein = "Carb"?:  The Inuit eat a fair amount of rotten meat.  This was the topic of inquiry in the initiating tweet that prompted the Eades interaction.  I was looking for information on bacterial decomposition of protein.  I don't have information to quantify this, but ammonia production in breakdown would indicate deamination and there are various indicators that lactic acid bacteria ferment amino acids.  This could produce things like lactate and proprionate that would contribute as stated previously or just amino acid derivatives that feed into Krebs as also discussed.  If the amino acids are pre-deaminated, this increases the amount of protein that can be consumed, and may convert some normally non-gluconeogenic amino acids to gluconeogenic substrates.
The purpose of ketogenesis is to provide an alternate fuel for glucose-dependent cells like those in the brain.  It only needs to do this to preserve protein stores.  So if there are sufficient gluconeogenic substrates around -- or molecules that can feed into the Krebs cycle -- there's less need for ketones.  It's as simple as that.  We can add to the above all of the glycerol released in lipolysis of fat stores to the pool of gluconeogenic substrates.   So long as the body can make glucose without catabolizing protein, there is no need for the ketones, and this would appear to be the case with the Inuit.  

4.  Genetic reasons why the Inuit weren't in nutritional ketosis:

Several months ago now, the IHC was abuzz over the CPT1A gene mutation in the Inuit (the study everyone cites talks about one region, so the prevalence may not be as high as reported).  Unfortunately, this was somewhat improperly interpreted leading to further misconceptions rather than fewer.  The "A" is the gene in the liver.  The liver is the only place (except for some activity in the kidney) where ketones are generated and released into circulation to be utilized (in Krebs in mitochondria) in other cells.

Fatty acid uptake into mitochondria is rather elegantly controlled by what is called the carnitine shuttle.  The way the body controls the movement of fatty acids is primarily keeping them bound in some way to some molecule or other so that they cannot simply pass through lipid membranes as their physico-chemical properties would allow.  Therefore, you have "carriers" escorting the FA-CoA through two membranes converting it to other moieties before being converted back to a FA-CoA to go into ß-oxidation and eventually Krebs.

This mutation would not allow sufficient fatty acid oxidation through the ß-oxidation pathway to form ketones.  However, the Inuit remain "fat burning beasts" because this mutation is localized in the liver.  If they could not burn fat for energy in the rest of their cells, they would die.  Period.   This mutation effects mostly children, especially young children.  A child with this mutation would require more glucose than the usual child as they are not capable of producing much of this alternate fuel which is also, apparently, a substrate for de novo lipogenesis of fatty acids for brain growth.    This mutation is associated with high infant mortality and therefore is relatively rare having been selected against in most humans.  Except the most northern climates ...

The Inuit infants still suffer both concurrent hypoketonemia and hypoglycemia, but if they make it through infancy, this is not an issue into adulthood.  The reasons here seem fairly straightforward.  A lot of glucose is needed for brain growth with ketones as either supplemental energy source and/or substrate for fatty acid synthesis.  That's a lot of glucose for a little liver to produce when it cannot produce ketones in the fasted state.  Later on, the liver is more than capable of producing sufficient glucose, and the Inuit diet as described above would indicate that they have sufficient substrate with which to do so.  The breastmilk of the Inuit may have two more unique fatty acid properties that allow these babies to survive:  (1) higher OCFA as previously discussed would enhance gluconeogenic substrate availability, and (2) higher very long chain PUFA content.  The latter is metabolized in peroxisomes and is found in few tissues in the human body, one being the brain.  

But some scientists have speculated further that the mutation is not just not selected out of the general population, but may have been selected for in the Inuit as it could be protective.  In T1 diabetics, ketosis runs out of hand due to the excessive FA supply to the liver.  There's no doubt that the circulating FA supply in the Inuit on a VLC diet would be high.  It may be protection against inappropriate ketogenesis that the mutation provides, but more likely it is protective of the mitochondria themselves.  You see, UCP2 activity is elevated in the fasted state, transporting excess FA's back out of the mitochondria.  In other words, it's not uncoupling/energy-dissipating like UCP1 in brown fat.  Impaired UCP2 is also one of the mitochondrial issues in those with genetic predisposition towards diabetes.  So ... the clamp on the "in" side provided by this mutation may well protect hepatocytes that would otherwise be susceptible to oxidative stress and all that mitochondrial nutritional overload jazz.

5. Ketosis doesn't really matter, the Inuit were fat burning beasts.

The above two paragraphs are observation-based hypotheses, nothing written in stone.  There's not much in terms of quantitating and testing available out there.   The take-away, however, is that it doesn't matter.  There is no evidence of the Inuit being in chronic (or even significant sporadic) nutritional ketosis.   There are copious accounts of periodic starvation ketosis when in late winter early spring stores would run out and the animals themselves are either hard to come by, or too lean to bother with.  Therefore, as I say here often, context is important.

The Inuit are IRRELEVANT to the question of whether the ketogenic diets being promoted within the IHC are healthy.   The diets bear little resemblence -- if any at all! -- to the foods that comprise the Inuit diet.  Both the types of foods and the nutritional profile of those foods are so different that it is dishonest to even represent the Inuit as any sort of "proof" about the healthfulness of the diet being advocated.

There are those who say that it's not important even if the Inuit are not in ketosis, they're still fat burning beastss and evidence that a high fat diet is healthy.  Note the moving of the goal posts as the keto-claims are dispelled.

So, to repeat, their diet is not nearly as high fat as it is routinely (and intentionally) misrepresented to be.  Furthermore, the quality of the fat in their diet mimics no paleo or LC diet out there.  It is highly UNsaturated.  Lastly, saying that a high fat diet is beneficial in a CPT1A-mutation-free person who goes into ketosis because it's healthy in a population with the mutation, is a lot like saying that a non-keto diet is fine for a GLUT1-deficient person.  Perhaps not a perfect analogy there, but we really do not know what the long term effects of running in nutritional ketosis are -- where the liver is constantly making ketones and glucose, the brain is trying to run on both with ketone delivery not even transporter mediated into the cells, and the rest of the body is dealing with an unnatural milieu of fuels from which to select.  The GLUT1-deficient person is helped immensely by a ketogenic diet (and they're looking into whether exogenous ketones might be a better solution given the side effects of the diet) because their brains do not take up adequate glucose.  There's no glut of glucose and ketones, just as the mitochondria of CPT1A deficient livers never see high glucose and fatty acids, and the brain and cells don't see high fatty acids and ketones.

To use the Inuit as examples of any aspect of a VLCKD/LCHF/Banting whatever diet is, to be blunt, to lie.  From the true nature of their diet to the peculiarities of their genetics, to the environment they live in.  Any which way you look at it, these ketowarriors are NOT like the Inuit.  Not even close.  If you want to promote the exact diet, complete with stomach contents of caribou and rotted seal meat, then you have a leg to stand on pointing to the Inuit diet.  Until then, you do not.

6.  Vilhjalmur Stefannson ate like an Inuit for a year and he was healthy.

Most have seen some version of the above slides and claims regarding Stefannson.  But per the last paragraph of the previous section, whatever Stefannson ate, it was not an Inuit diet.  He did not have caribou and seal meat flown in, no, he ate meat and organs of domestic livestock and poultry.  So I suppose he is the poster boy for the zero carb carnivore types to some extent.  But this experiment is n=1 and case study, and here's why it is largely irrelevant:
  • The experiment was undertaken by three men, one stopped after 10 days.
  • The diet could be verified for the first ~2 months of the year it lasted. The men did not even check back into the hospital for the end-of-year examinations.
  • The high protein diet was attempted for a few days, made them sick, and was abandoned for a diet of about 75% fat.  No attempt appears to have been made to transition to more Inuit-appropriate ratios.  
  • I don't know how infamous Stefannson was, but doubtful the other man involved would be recognized on the street.  There really is no way to verify that the diet was followed strictly for an entire year.
  • No women.
  • It was only a year.
When well nourished people undertake extreme restrictions of one sort or another, it may take longer than a year to deplete the body's stores of certain nutrients, and longer still for deficiencies to manifest themselves.  Thus we are left to those who promote eating only meat and limited verifiable information as to the whole of the impact on their health and well being.

7.   No long term RCTs for VLC or ketogenic diets

There are several diet comparison clinical trials lasting up to a year or two, and even a few with follow up to six years.  Most notably the Shai study in Israeli business (mostly) men.  This is the study that Teicholz claims is the be all and end all of awesomesauceness RCT perfection (see here, with links to other relevant posts).   NONE of the diets in these one and two year studies were anywhere close to < 50 grams carb per day generally accepted as VLC, or < 20 grams carb per day often required for "nutritional ketosis".  Perhaps more importantly, the fat intake in Shai LC arm was around 40%.  Expressing fat intake as a percent is misleading anyway, as what really needs to be done is a trial maintaining (weight stable) a large number of people on such a diet to demonstrate it to be nutritionally adequate and beneficial to health.  

8.  Lack of evidence for "nutritional ketosis" in short-term RCTs

In the absence of long term studies, the next goal post moving fall back position is the short term trials.  There have been many.  Again, most are not even VLC or VLCKD for the duration of these trials.

It's actually kind of interesting looking back to 2010 and a book called The New Atkins for a New You by Eric Westman MD, Jeff Volek PhD and Stephen Phinney MD,PhD.   While the original Atkins book was virtually ALL about the ketosis, the updated version barely mentions it.  While the term "nutritional ketosis" makes it into the lexicon, there is no indication that ketosis is even required for weight loss, or a state to be monitored, etc.  Perhaps it is because at that point (and long before) this trio knew that ketones weren't the magical key to a low carb diet.  They wrote the following 2007 paper in the American Journal of Clinical Nutrition:  Low-carbohydrate nutrition and metabolism  (authors:  Eric C Westman, Richard D Feinman, John C Mavropoulos, Mary C Vernon, Jeff S Volek, James A Wortman, William S Yancy, and Stephen D Phinney)
The role of ketogenesis
Ketone concentrations after LCD intake have now been measured in several studies. In a study of persons with type 2 diabetes, urinary ketone body excretion increased from a mean of 0.10 mmol/d at the end of the usual diet to a peak of 2.75 mmol/d after 1 wk of the LCKD (P < 0.001); it then decreased gradually for a week but remained above baseline (13). The mean plasma total-body ketone concentrations were 130 mol/L (91.5% ß -hydroxybutyrate) at the end of the usual diet and increased 5-fold to 653 mol/L (97.4% ß-hydroxybutyrate) at the end of the LCKD (P < 0.001). Two longer-term studies, in persons without diabetes, that measured fasting blood ß -hydroxybutyrate concentrations over 10 wk found that, whereas the concentrations increased over the first 2 – 4 wk, they then decreased and, after 10 –12 wk, remained only slightly higher than those of dieters following other diets (21, 23).
Ref 21 (2007, LC was 4% carb) 

Ref 23 (2004, LC was ~60g = 15% carb)  

It is important to keep in mind that folks like Jeff Volek were referring to low carb diets (usually around under 50 grams or < 15%) as VLCKDs, and many of these diets -- often employed in their own research -- were quite high in protein. 

Look at the ketones even in the initial period, the spike.  Now here's what is said in Volek & Phinney's books:
To achieve optimal fuel flow during keto-adaptation you should aim for blood ketone levels between 0.5 and 3.0 millimolar.  Phinney, Stephen; Volek, Jeff (2012-06-15). The Art and Science of Low Carbohydrate Performance (p. 89). Beyond Obesity LLC. Kindle Edition. 
A unit check, 0.5 millimolar is 500 micromolar, the above plots are in millimolar (top) and μmolar (bottom) -- neither even "spikes" into "nutritional ketosis".   Thus, even initially, many of the studies often cited in support of NuttyK do not even qualify.

Jumping forward to 2014, and a study Phinney was involved in assessing a keto diet in diabetics.  This was the Saslow study blogged on here, a 12 week study where the 11 keto subjects tested blood ketones twice a week.  
At week 4, when most participants should have transitioned into nutritional ketosis, 55% (6/11) reported a level of at least 0.5 mM and 73% (8/11) reported a level of at least 0.3 mM. By week 6, 75% (9/11) reported a level of at least 0.5 mM and 92% (11/12) reported a level of at least 0.3 mM.
How about at week 8, or week 12?  Nope.  Not reported.  What is one to make of that?  This is what is so frustrating about research coming out of clearly biased agenda-driven researchers.  Likely by week 12, most were reporting levels under 0.5 mM and providing this information would have countered the implication that the nominal ketosis itself was responsible for glycemic improvements.   But were these folks even in nutritional ketosis for a full 12 weeks?  Furthermore, ketones were apparently not assessed at all in the MCCR group, which would be a reasonable expectation for comparison.   Thus even the newfound interest in ketogenesis hasn't really made it into the clinical testing protocols.

Whatever metabolic changes (usually improvements) in short term studies -- particularly in the hypocaloric weight loss context -- cannot be extrapolated to infer ANY long term benefits or claims of healthfulness.  If you believe they do, then Mark Haub and Fat Head Naughton have shown us that eating junk food in mild caloric deficit and losing weight means junk food is a perfectly healthy long term diet in a weight maintaining state.  Heck ... maybe it is ;-)

SUMMARY Points 1 thru 8

The bottom line, for all of the hand-wringing and hair pulling over how the "low fat diet" is not based on science, and is potentially dangerous, is that this charge is far more appropriately leveled at low carb diets, those "well designed" to evoke a chronic state of "nutritional ketosis". 

  • No observational data from traditional cultures assessing health outcomes because the diet doesn't even exist!
  • No long term RCTs at all
  • Few relevant short term RCTs that cannot be extrapolated to long term.

This is why, as unverifiable as it all is, the outcomes of the proponents of such diets become relevant.  Ketogenic diets are the key to lifelong sveltitude and youthfully exuberant health?   Healthy?  Each can pass their own judgments on that, I'd say it doesn't look very good when the gurus and book authors look more like they should be seeking out advice from others, and they're often worse off than before adopting their "healthy" diet.  Unfortunately, this side is not often revealed, or is "confessed" long after advocating for exactly the dietary practices that ended up impacting them negatively.  Sigh...

Which brings us to ...

9.  Keto for Epilepsy

In the standard course of learning about low carbohydrate diets, it doesn't take long before the use of ketogenic diets in the treatment of epilepsy enters the conversation.  Indeed, despite the fact that The New Atkins (2010) makes no mention about targeting ketosis inconjunction with effective fat loss, the forward of the book was written by Eric Kossoff MD.    Kossoff is is the director of the Ketogenic Diet Center for the treatment of epilepsy at Johns Hopkins.  He is also a fellow member -- along with Volek and Phinney -- of the Atkins Nutritionals Scientific Advisory Board, and from his glowing endorsement of the three authors of the book and exaggerated glorification of the supposed superiority of low carb diets, one gathers he's a fan of the Atkins diet for obesity and diabetes.

Back in 2010 I read TNA, but hadn't had access to the book for a few years since it was in a reader/service I no longer used for various reasons.  At the time, I pretty much read epilepsy ... went "yada yada, irrelevant" in my head ... and skipped to the meat of the book.  So I recognized the name, knew the man from the Atkins website, but had never really read much written or spoken by him before obtaining a copy of this book:   Ketogenic Diets: Treatments for Epilepsy and Other Disorders.  My reason for doing so was prompted by the keto craze, and to see what someone involved in using ketogenic diets in a clinical setting had to say about long term safety, etc.  Even though such diets had little relevance to most low carb plans, they should be somewhat more relevant to the new ketogenic versions being popularized by Peter Attia and Jimmy Moore ostensibly adopting the Volek & Phinney protocol for nutritional ketosis.  

My take-aways from the book were:
  • Don't try this at home.  (IOW this should be medically supervised)
  • Beware of the side effects, follow the advice to mitigate, etc.
  • Get in, realize the therapeutic effect, then get out!  
Here's an important passage:
Even in super successful cases, most centers will start seriously considering the risks of the diet compared to benefits after 2 years. In many children, we suspect the diet has “done its job” and without it seizures will be no different than with it.  The only way to find out ultimately is to wean the diet!
Read that again.  As many times as needed to grasp the FACT that keto is for therapeutic effect for a definable condition.  Even when it has produced the therapeutic effect, or perhaps especially so, the risk/benefit analysis of continuing the diet needs to be reassessed.   Before continuing,  I would also like to point out that the keto diet for kids -- even when adhered to -- is by no means a magical silver bullet.  I realize this post has been reference link sparse, but I feel the following study is important for context:  The Ketogenic Diet: A 3- to 6-Year Follow-Up of 150 Children Enrolled Prospectively ... also because this study was conducted at Johns Hopkins.  There seems to be a romanticizing of keto as if it is a miracle cure for all.  The numbers tell a different story.  Yes, it is still a promising one and the reason why keto is embraced by the medical establishment for epilepsy treatment:  it's been demonstrated to work.  And yet, like many other medical (pharmaceutical included) interventions, it is far from 100% effective, and not without side effects.  So below are two summary tables form this study (that link is to freely available full text for anyone seeing further details).

Here's a run down on keto on an epilepsy website with some info (Kossoff co-author).  I found the information surprisingly accurate for those who don't wish to chase down all the particulars of a true keto diet:  

From Kossoff's book:
Preliminary evidence using blood ketones suggests that once the blood ketone level rises to more than 2 mmol, the urine ketone level becomes 4+. That is the highest level the dipsticks can measure. Seizure control however, appears far better when serum levels are greater than 4 mmol, way beyond that 4+ urine level. So, a urine ketone test of 4+ is necessary to establish that the child has ketosis but not sufficient to indicate very good ketosis.


  • Even for the proven treatment of epilepsy, ketogenic diets are not always effective, and often are still accompanied by medications.
  • Keto is not forever, mean duration around 2.5 years
  • Keto is a VERY restrictive diet:  It is calorie and carb/protein controlled and menus are carefully calculated and planned out.  Foods outside meals?  One or two nuts, 25 grams of lettuce, 3 olives.  
  • Ketosis for seizure relief is generally on the higher end of "nutritional ketosis" 4 mmol.  Look back again at the ketones in the "keto low carb vor weight loss and other stuff" studies ...
  • There are side effects.  Some can be mitigated, some are undertaken on a balancing of risk vs. benefit basis.

What about Modified Atkins?

The folks at Johns Hopkins have done some testing of MAD for epilepsy based on reports of children either adopting the diet when keto was too strict, or going on the diet with parental guidance even before trying keto.  It works for some.  It comes out high protein as a percentage.  MAD is essentially < 10 g carb/day "induction".  In children it has worked for, measured ketones are "large".    So there may be some metabolisms that are more prone to producing ketones than others.  This is still not likely to be a high protein -- in absolute amounts -- diet.  

10.  NuttyK vs. True Keto: A Two-Way Context Problem

For those not living under a rock in the IHC, ketowars have been raging for a while.  As it turrns out, NuttyK is somewhere between your standard VLC diet and a true therapeutic ketogenic diet (I'll dub it a TKD).  So in this final section I'll point out that context is important, and that contextual importance is a two-way street.  The proponents of NuttyK like to point to clinical benefits of TKDs as evidence in support of its healthfulness and effectiveness while resting on whatever clinical laurels the VLC diets offer.  The opponents of NuttyK have recently coalesced behind the Paleo Mom, Sarah Ballantyne.  Ballantyne has been "speaking out" at paleo conferences and on her podcast for several months now -- much to the frustration of Keto Warrior Moore.  Recently, with support in the literature review from Denise Minger, Ballantyne published a review of the literature in support of her positions.  Mostly this highlights the downside of such diets and details negative side effects and the need for medical supervision.  The problem here is the same, however.  It is a valid criticism to level that NuttyK actually isn't nearly as extreme as a TKD after all.

You cannot have it both ways.

The 80% fat diets being promoted by the current keto crowd do resemble TKDs in one way:  they are 4:1 fat:(pro+carb).  They are not, however, calorie restricted and carefully planned out like the TKD is, even if you scaled some of the kid diets up to adult (even though normal kids do eat a lot) intakes.  Still, at around that fat level, food choices become restricted and it is very easy to find oneself consuming a nutritent deficient diet.  Further, many of the complications seen with TKDs have shown up in folks on NuttyK.  Ballantyne is in a conundrum because unfortunately there are no studies on the long term -- two, three, even five year -- effects of chronic carbohydrate restriction:  aka metabolic starvation.  And so those who develop "adrenal fatigue" unfortunately cannot find much in the scientific literature so they make up fake syndromes.  This of course gives opportunities to sell a $200 program to fix your situation, or you could suggest people eat some actual carbohydrate.  

Sadly, those who promote this diet don't really have any direct comparative evidence to substantiate their claims.


Despite the rhetoric of those like Adele Hite, Zoe Harcombe and Nina Teicholz, the American diet has changed inconsequentially in the past 50 years in terms of macronutrient composition.  Furthermore, the supposed changes still leave the diet in the US at much higher fat levels than most cultures around the globe.  Furthermore, contrary to the lore of the IHC, it is far easier (and I do mean by a wide margin) to find examples of cultures subsisting on under 20% fat than it is to find one consuming over 80% fat.  We're talking habitual intake.  The latter doesn't even exist.

So the USDA Dietary Guidelines were never some unscientific crazy and dangerous gamble to suggest on a population-wide basis.  Ornish would be.  The Food Pyramid or My Plate or whatever?  No.  Sorry, that dog don't hunt, and all that.  You do not need long term randomized controlled clinical trials to test diets that are verifiably habitually consumed by humans, and in many cases, have been for centuries.

So what is the agenda of those who rail against the Guidelines?  Who seek to have them revoked?  Is it to replace them with LCHF?  The onus is on THEM to provide the evidence they say is lacking for current recommendations.  To that end, can you point to any culture and their health outcomes?  NO.  Do you have any long term RCTs?  NO.  

Get back to me when you do.  Until that time, it is irresponsible to promote such diets as healthy, especially when they don't appear to be so with those who advocate most fiercely!

Nutritional ketosis is an oxymoron.  There is no evidence that this state is even desired, let alone optimal or even safe over the long term.


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