Ketogenic diet basics - Paul Jaminet, Ph.D & Shou-Ching Shih Jaminet, Ph.D

from the Perfect Health Diet blog:


Part 1 - Summary

Ketogenic Diets, I: Ways to Make a Diet Ketogenic | Perfect Health Diet

Three ways to make the diet ketogenic:

1)      Make Wilder’s “ketogenic ratio” high by eating a lot of fat, very few carbs, and not too much protein.
2)      Supplement with the ketogenic amino acids lysine and leucine.
3)      Supplement with coconut oil or another source of short-chain fats.

If we do (2) or (3), then the diet can be ketogenic even if it has a fair number of carbs.

So now we have an arsenal of ways to generate ketones. We have to look at diseases and diet risks to figure out which way of making the diet ketogenic is optimal.


Part 2 - Summary

 Ketogenic Diets 2: Preventing Muscle and Bone Loss on Ketogenic Diets | Perfect Health Diet

I believe the extreme limits on carb and protein intake in conventional clinical ketogenic diets are responsible for their growth stunting, muscle destroying, fattening effects.

In order to supply sufficient protein and carbs while maintaining ketosis, it is necessary to provide ketogenic short-chain fats and amino acids.

Clinical testing of such supplemented diets has so far produced encouraging results. Providing supplemental amino acids to epileptic children on ketogenic diets improved their health and allowed them to maintain ketosis with higher protein intake. Seizure frequency was reduced even as side effects diminished.

Personally, I wouldn’t attempt a long-term ketogenic diet without the aid of coconut oil (or MCTs), lysine, and the branched chain amino acids.

For the NBIA/PKAN kids, it seems that the amino acid supplements should be some mix of lysine, leucine, isoleucine, and valine, with the isoleucine and valine included solely to reduce leucine toxicity. The optimal amount of isoleucine and valine should be smaller than is found in branched-chain amino acid supplements, since leucine by itself may help prevent iron accumulation and increase ketosis. Also, one rat study [4] indicates that isoleucine alone, excluding valine, might be enough to relieve leucine toxicity. Excluding valine would increase the ketogenicity of the supplement mix.

I think the NBIA/PKAN kids will need to experiment with primarily lysine and leucine, and secondarily isoleucine and BCAA supplements, to see what mix works best for them.



[1] Owen OE et al. Brain metabolism during fasting. J Clin Invest. 1967 Oct;46(10):1589-95. http://pmid.us/6061736.
[1] Groesbeck DK et al. Long-term use of the ketogenic diet in the treatment of epilepsy. Dev Med Child Neurol. 2006 Dec;48(12):978-81. http://pmid.us/17109786. Hat tip CarbSane.
[2] Ribeiro LC et al. Ketogenic diet-fed rats have increased fat mass and phosphoenolpyruvate carboxykinase activity. Mol Nutr Food Res. 2008 Nov;52(11):1365-71. http://pmid.us/18655006. Hat tip CarbSane.
[3] Evangeliou A et al. Branched chain amino acids as adjunctive therapy to ketogenic diet in epilepsy: pilot study and hypothesis. J Child Neurol. 2009 Oct;24(10):1268-72. http://pmid.us/19687389. Hat tip Nigel Kinbrum.
[4] Tsubuku S et al. Thirteen-week oral toxicity study of branched-chain amino acids in rats. Int J Toxicol. 2004 Mar-Apr;23(2):119-26. http://pmid.us/15204732.
[5] Yudkoff M et al. Brain amino acid requirements and toxicity: the example of leucine. J Nutr. 2005 Jun;135(6 Suppl):1531S-8S. http://pmid.us/15930465.
[6] Mawatari K et al. Prolonged oral treatment with an essential amino acid L-leucine does not affect female reproductive function and embryo-fetal development in rats. Food Chem Toxicol. 2004 Sep;42(9):1505-11. http://pmid.us/15234081.
[7] Tsubuku S et al. Thirteen-week oral toxicity study of L-lysine hydrochloride in rats. Int J Toxicol. 2004 Mar-Apr;23(2):113-8. http://pmid.us/15204731.
Ketogenic Diets | Perfect Health Diet

High cholesterol - comes with better memory in aged

Evolutionary Psychiatry: Nutrition and Alzheimer's Disease - Dangers of Insulin Resistance and Low Cholesterol
"…high cholesterol level is positively correlated with longevity in people over 85 years old, and in some cases has been shown to be associated with better memory function and reduced dementia… the cerebrospinal fluid of [Alzheimer's Disease] patients is substantially depleted in lipoproteins, cholesterol, triglycerides, and free fatty acids compared to matched controls."

We know that there is a strong correlation between insulin resistance and early Alzheimer's, and also there is an association between mitochondrial dysfunction (particularly in complex 1) and Alzheimer's. As I discussed in Basic Science: Energy is Everything and Brain Efficiency, when the mitochondria aren't happy, your brain isn't happy. Mitochondrial dysfunction is also implicated in Parkinson's Disease and ALS, both long-term and ultimately fatal degenerative conditions.

And now, a point I've made before (in Low Cholesterol and Suicide)- the brain is relatively small, but has 25% of the body's cholesterol. Cholesterol insulates neurons as part of the myelin sheath and provides the scaffold for the neural network, and is an important part of the membranes and all synapses. While much of the cholesterol used in the brain is made in the brain, there is clear evidence that apolipoprotein E (ApoE) is a big player in the game of shuttling cholesterol, fat, and antioxidants to the central nervous system from the body's main cholesterol factory, the liver. ApoE is made in nerve cells called astrocytes (who tend to and feed neurons), and ApoE allows the astrocytes to suck lipids, antioxidants, and cholesterol arriving in LDL and IDL particles from the bloodstream. Yes, astrocytes can transport LDL across the blood brain barrier.

The biggest genetic risk for Alzheimer's is being a carrier of a certain type of ApoE gene called ApoE4. Research has shown that ApoE4 is associated with reduced cholesterol uptake by the astrocytes. What has been confusing for the lipophobic medical establishment is that ApoE4 is associated with high LDL cholesterol… so it must be that nasty horrible LDL killing the brain! But the key bit to understand is that LDL cholesterol in longitudinal studies tends to drop before the development of Alzheimer's disease. Hmmm. We can't ignore the following tantalizing clue either:

…high cholesterol level is positively correlated with longevity in people over 85 years old, and in some cases has been shown to be associated with better memory function and reduced dementia… the cerebrospinal fluid of [Alzheimer's Disease] patients is substantially depleted in lipoproteins, cholesterol, triglycerides, and free fatty acids compared to matched controls.
All of us, but especially readers of a since-removed blog post that was part of the Venus-gate paleo disruption of a few weeks ago about the supposed dangers of densely packed saturated fat should have an understanding of how lipoproteins work. Lipoproteins (such as HDL, LDL, chylomicrons, and VLDL) basically look like this:

Image from Wikipedia

Lipoproteins carry fats and other delicacies through the blood. The blood is dangerous and filled with nasty things like oxygen and iron that can break down our gentle fats. We don't want our fats oxidized - so the lipoproteins tuck the fats into the inside to keep them safe and snuggly. Again, a MAJOR REASON for the particular structure of lipoproteins is to keep those fats safe and not exposed to the blood. Once fats are delivered to cell membranes, we still want to keep them safe - and cholesterol is like a bit of plate armor - it helps the fats stack more tightly, protecting them from oxidative damage and invading microbial pathogens.

Seneff et al continue to stack the evidence in their paper - dietary avoidance of fat (replaced by carbohydrate) and the increasingly zealous prescriptions for cholesterol-lowering medication has coincided with the rise in Alzheimer's Dementia and diabetes and obesity. These are only correlations, but one might consider that to be some evidence in favor of the plausible hypothesis that stripping the brain of cholesterol especially in an oxidative, hyperglycemic environment could lead to very sick neurons.

The Cochrane Collaboration - Library resources

great resource library, specifically open to the lay as well as the professional researcher.......

Cochrane Reviews - Alphabetically: [A]

About The Cochrane Library - The Cochrane Library

Home - The Cochrane Library

About us | The Cochrane Collaboration

"Our vision is that healthcare decision-making throughout the world will be informed by high quality, timely research evidence"

"The Cochrane Collaboration, established in 1993, is an international network of people helping healthcare providers, policy makers, patients, their advocates and carers, make well-informed decisions about human health care by preparing, updating and promoting the accessibility of Cochrane Reviews – over 4,500 so far, published online in The Cochrane Library. 
We believe in equal partnerships
The Collaboration believes that effective health care is created through equal partnerships between researcher, provider, practitioner and patient.
Cochrane Reviews are unique because they are both produced by, and are relevant to, everyone interested in the effects of health care. Based on the best available evidence, healthcare providers can decide if they should fund production of a particular drug. Practitioners can find out if an intervention is effective in a specific clinical context. Patients and other healthcare consumers can assess the potential risks and benefits of their treatment."

Study (2011) - no evidence that carbohydrates improve cognition in the aged

Carbohydrates for improving the cognitive performance of independent-living older adults with normal cognition or mild cognitive impairment

Plain Language Summary

There is no available evidence to support the use of any form of carbohydrate to improve cognitive performance in older adults with normal or mild cognitive impairment.

Carbohydrates consist of sugars, oligosaccharides, and polysaccharides. These components are found in a large range of foods in the diet and have variable effects on digestion, blood sugar levels, and impacts on health. Despite the evidence accumulated from biological and epidemiological studies and non-randomised clinical trials, there are still no randomised, controlled trials for analysing the efficacy and safety of carbohydrates in improving cognitive performance in this review. Thus, we need more studies on different types of carbohydrates, particularly those from fruit, vegetable and whole grain sources, for older adults with normal cognition and mild cognitive impairment in order to understand the role of this nutrient in the prevention or reduction of cognitive decline.



Mild cognitive impairment (MCI) is an intermediate state between normal cognition and dementia in which daily function is largely intact. This condition may present an opportunity for research into the prevention of dementia. Carbohydrate is an essential and easily accessible macronutrient which influences cognitive performance. A better understanding of carbohydrate-driven cognitive changes in normal cognition and mild cognitive impairment may suggest ways to prevent or reduce cognitive decline.


To assess the effectiveness of carbohydrates in improving cognitive function in older adults.

Search strategy

We searched ALOIS, the Cochrane Dementia and Cognitive Improvement Group Specialized Register on 22 June 2010 using the terms: carbohydrates OR carbohydrate OR monosaccharides OR disaccharides OR oligosaccharides OR polysaccharides OR CARBS. ALOIS contains records from all major healthcare databases (The Cochrane Library, MEDLINE, EMBASE, PsycINFO, CINAHL, LILACS) as well as from many trial databases and grey literature sources.

Selection criteria

All randomised controlled trials (RCT) that have examined the efficacy of any form of carbohydrates in normal cognition and MCI.

Data collection and analysis

One review author selected and retrieved relevant articles for further assessment. The remaining authors independently assessed whether any of the retrieved trials should be included. Disagreements were resolved by discussion.

Main results

There is no suitable RCT of any form of carbohydrates involving independent-living older adults with normal cognition or mild cognitive impairment.

Authors' conclusions

There are no suitable RCTs on which to base any recommendations about the use of any form of carbohydrate for enhancing cognitive performance in older adults with normal cognition or mild cognitive impairment. More studies of many different carbohydrates are needed to tease out complex nutritional issues and further evaluate memory improvement.

More fat less carb is best - recent Studies

That Paleo Guy: Low Carbohydrate Diet Review: Shifting the Paradigm

"For those of us who have been on board with, and operating under this paradigm for some time now, there is really nothing new at all in this review. However, it does provide a good summary of all of the common issues and concerns around low-carbing, particular those that are often put forward by clinician's themselves. There is the nod, in this review, to the fact that these clinicians are clinging to a wisdom and practise that is protective of their own beliefs and biases rather than focused on the patient. As suggest by the authors, you can advocate all the low glycaemic index breads you like as a way to manage diabetes, for example, but the glucometer doesn't lie.

Is this a game changer? Doubt it. As I mentioned in my introduction, I have had health professionals tell me that they would only consider a change in clinical approach if I could provide a solid meta-analysis or Cochrane review (obviously thinking I couldn't). When such evidence is produced, it still isn't enough and other reasons as to why 'the science' is wrong come to the fore (clinical best practise seems to be a matter of faith rather than physiology and commonsense). However, there will be those clinicians who have perhaps been sitting on the fence with this paradigm and who just haven't had the time to do an in-depth review around all the common issues. This paper is for them, and may just be enough to knock them off the fence and onto the low carb side. More importantly, this paper, with its ease of reading, is for the patient. There isn't a lot in here that would bog a patient down, and for clinicians wanting to take their patient down the low carb pathway (maybe by applying paleo principles), this could be the ideal review to pass on to their patient to give them confidence in that pathway.

This review isn't going to create a seismic shift in paradigm, but it is certainly building pressure and rumbling in the right direction."

Study (2010) - doubts saturated fat causes heart disease

Meta-analysis of prospective cohort studies evalua... [Am J Clin Nutr. 2010] - PubMed result

Am J Clin Nutr. 2010 Mar;91(3):535-46. Epub 2010 Jan 13.

Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.


Children's Hospital, Oakland Research Institute Oakland, CA, USA.



A reduction in dietary saturated fat has generally been thought to improve cardiovascular health.


The objective of this meta-analysis was to summarize the evidence related to the association of dietary saturated fat with risk of coronary heart disease (CHD), stroke, and cardiovascular disease (CVD; CHD inclusive of stroke) in prospective epidemiologic studies.


Twenty-one studies identified by searching MEDLINE and EMBASE databases and secondary referencing qualified for inclusion in this study. A random-effects model was used to derive composite relative risk estimates for CHD, stroke, and CVD.


During 5-23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results.


A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.

Study (2007) disputes "wholegrain for heart health"

Wholegrain cereals for coronary heart disease  

by the Cochrane Collaboration

[Plain Language Summary]

Wholegrain foods encompass a range of products and examples are wholegrain wheat, rice, maize and oats. The term wholegrain also includes milled wholegrains such as oatmeal and wholemeal wheat.

The evidence found by this review is limited to wholegrain oats, and to changes in lipids as an outcome. There is a lack of studies on other wholegrain foods or diets. There is some evidence from this review that oatmeal foods can beneficially lower lipid levels such as low density lipoproteins (LDL) cholesterol and total cholesterol in those previously diagnosed with risk factors for coronary heart disease (CHD) even with relatively short interventions. However, the results should be interpreted with caution because the trials found are small, of short duration and many were commercially funded. No studies were found that reported the effect of wholegrain foods or diets on deaths from, or occurrence of CHD.

This is a Cochrane review abstract and plain language summary, prepared and maintained by The Cochrane Collaboration, currently published in The Cochrane Database of Systematic Reviews 2011 Issue 6, Copyright © 2011 

The Cochrane Collaboration. Published by John Wiley and Sons, Ltd.. The full text of the review is available in The Cochrane Library (ISSN 1464-780X).

This record should be cited as: Kelly SAM, Summerbell CD, Brynes A, Whittaker V, Frost G. Wholegrain cereals for coronary heart disease. Cochrane Database of Systematic Reviews 2007, Issue 2. Art. No.: CD005051. DOI: 10.1002/14651858.CD005051.pub2

Editorial Group: Heart Group

This version first published online: April 18. 2007


Omega 6 bad, omega 3 good - major (2010) study

Food and Behaviour Research: Ramsden CE et al 2010 - n-6 Fatty acid-specific and mixed polyunsaturate dietary interventions have different effects on CHD risk: a meta-analysis of randomised controlled trials

Web URL: View this and other related abstracts on PubMed here

Lay Summary:


These findings indicate that dietary advice to consume more 'polyunsaturated fats' (PUFA) by using vegetable oils to replace solid fats like butter, lard or hard margarines may actually increase the risk of heart disease if the vegetable oils only contain omega-6 PUFA.

Previous studies relating dietary fat intake to heart health have failed to consider the very different effects of omega-6 versus omega-3 PUFA. (Broadly speaking, omega-6 PUFA tend to promote inflammation and blood clots, whereas omega-3 PUFA have the opposite effects).

These findings, published in the British Journal of Nutrition, are based on a detailed re-analysis of results from placebo-controlled treatment trials involving over 11,000 people in total. This time, the scientists carefully separated the studies in which the dietary treatments contained omega-6 PUFA only, or a mixture of omega-3 and omega-6 PUFA.

Only the 'mixed omega-3 and omega-6 PUFA' trials showed any benefits in reducing heart disease risk. By contrast, the use of omega-6 PUFA alone was associated with slightly worse heart disease outcomes.

Omega-3 PUFA have repeatedly been shown to have benefits for heart health, but it is the longer-chain forms (EPA and DHA) - found in oily fish and seafood - which are the most valuable for heart health (as well as for the brain and immune system). Only a few vegetable oils (such as flaxseed oil, rapeseed oil, or soybean oil) contain any omega-3 PUFA - although this is in a shorter-chain form (alpha-linolenic acid) that is not as beneficial to human health as EPA and DHA. Many of the most commonly used vegetable oils (such as corn oil, sunflower oil or safflower oil) are high in omega 6 PUFA, and contain no omega-3 PUFA at all.


Randomised controlled trials (RCT) of mixed n-6 and n-3 PUFA diets, and meta-analyses of their CHD outcomes, have been considered decisive evidence in specifically advising consumption of 'at least 5-10 % of energy as n-6 PUFA'. Here we

(1) performed an extensive literature search and extracted detailed dietary and outcome data enabling a critical examination of all RCT that increased PUFA and reported relevant CHD outcomes;

(2) determined if dietary interventions increased n-6 PUFA with specificity, or increased both n-3 and n-6 PUFA (i.e. mixed n-3/n-6 PUFA diets);

(3) compared mixed n-3/n-6 PUFA to n-6 specific PUFA diets on relevant CHD outcomes in meta-analyses;

(4) evaluated the potential confounding role of trans-fatty acids (TFA).

n-3 PUFA intakes were increased substantially in four of eight datasets, and the n-6 PUFA linoleic acid was raised with specificity in four datasets. n-3 and n-6 PUFA replaced a combination of TFA and SFA in all eight datasets.

For non-fatal myocardial infarction (MI)+CHD death, the pooled risk reduction for mixed n-3/n-6 PUFA diets was 22 % (risk ratio (RR) 0·78; 95 % CI 0·65, 0·93) compared to an increased risk of 13 % for n-6 specific PUFA diets (RR 1·13; 95 % CI 0·84, 1·53). Risk of non-fatal MI+CHD death was significantly higher in n-6 specific PUFA diets compared to mixed n-3/n-6 PUFA diets (P = 0·02).

RCT that substituted n-6 PUFA for TFA and SFA without simultaneously increasing n-3 PUFA produced an increase in risk of death that approached statistical significance (RR 1·16; 95 % CI 0·95, 1·42).

Advice to specifically increase n-6 PUFA intake, based on mixed n-3/n-6 RCT data, is unlikely to provide the intended benefits, and may actually increase the risks of CHD and death.

Goodbye CutTheCarb - another ex low-carber

Goodbye CutTheCarb

Goodbye CutTheCarb

In 2007, put into motion by personal experiences, I started my search for THE overweight and disease exiling diet. I investigated and tried supposed health bringing supplements, raw food, vegetarianism and more.

In the beginning of 2008 I read Gary Taubes’ book Good Calories Bad Calories. This book shifted my paradigm (and that of so many others). I probably misinterpreted it in those days, but it made me so carbophobic that I practically eliminated all carbohydrates from my diet. I mainly ate meat, fish, eggs, coconut oil and butter. And I surely lost weight, but in the long run I also got starvation symptoms like irritability and shakiness.

After years of self-studying biology and physiology and reading a lot of blog posts, books and scientific publications I have come to the conclusion that when you’re not diabetic or metabolically derailed you can safely consume reasonable quantities of carbohydrates. Reasonable is somewhere between 15 and 30 percent of your calories; this as long as you match your calorie intake with your level of activity. Starch, which consists of mainly glucose, is the preferred carbohydrate. Fructose, fructan and lactose can best be firmly restricted.

Of course I brought this insight into practice and it resulted in a desired weight gain mainly coming from extra muscle. Adding about 100 net grams of carbs very much improved my body composition. Also the irritability and shakiness disappeared.

Observational Studies, association and causality

Nothing wrong with Observational Studies. And Association does Imply Causality but… « Richard David Feinman

Nothing wrong with Observational Studies. And Association does Imply Causality but…

Posted: June 19, 2011 by rdfeinman in Association and Causality, Evidence Based Medicine, Intention to Treat, low-carbohydrate diet, Observational Studies, thermodynamics
Tags: , ,

…the association has to be strong and the causality has to be plausible and consistent. And you have to have some reason to make the observation; you can’t look at everything. And experimentally, observation may be all that you have — almost all of astronomy is observational. Of course, the great deconstructions of crazy nutritional science — several from Mike Eades blog and Tom Naughton’s hysterically funny-but-true course in how to be a scientist – are still right on but, strictly speaking, it is the faulty logic of the studies and the whacko observations that is the problem, not simply that they are observational. It is the strength and reliability of the association that tells you whether causality is implied. Reducing carbohydrates lowers triglycerides. There is a causal link. You have to be capable of the state of mind of the low-fat politburo not to see this (for example, Circulation, May 24, 2011; 123(20): 2292 – 2333).

It is frequently said that observational studies are only good for generating hypotheses but it is really the other way around. All studies are generated by hypotheses. As Einstein put it: your theory determines what you measure. I ran my post on the red meat story passed April Smith and her reaction was “why red meat? Why not pancakes” which is exactly right. Any number of things can be observed. Once you pick, you have a hypothesis.

Dietary Guidelines Committee Receives The Spanking It Deserves

Fat Head » The Dietary Guidelines Committee Receives The Spanking It Deserves

The journal Nutrition just published a paper titled In The Face Of Contradictory Evidence: Report Of The Dietary Guidelines For Americans Committee. The authors are Adele Hite, MAT; Richard Feinman, PhD; Gabriel Guzman, PhD; Morton Satin, MSc; Pamela Schoenfeld, RD; and Richard Wood, PhD.

Sure, a lot of bloggers ripped the 2010 Dietary Guidelines for spouting the same old nonsense, but we’re bloggers, not academic researchers, so we’re easy to ignore.

It’s not so easy to dismiss this group, especially when their paper is published in a respected journal. This paragraph from the abstract pretty much sums it up:

Although appealing to an evidence-based methodology, the DGAC Report demonstrates several critical weaknesses, including use of an incomplete body of relevant science; inaccurately representing, interpreting, or summarizing the literature; and drawing conclusions and/or making recommendations that do not reflect the limitations or controversies in the science.

In fact, the topic headings in the paper read like a list of charges. Here are few sample headings:

Macronutrients: Research questions are formulated in a way that prevents a thorough investigation of the literature

Macronutrients and weight loss: Science is inaccurately summarized

Low-carbohydrate diets: Science is inaccurately represented

Low-carbohydrate diets: Conclusions do not reflect quantity and/or quality of relevant science

Effects of saturated fat: Answers based on an incomplete body of relevant science

Effects of saturated fat: Science is inaccurately represented or summarized

Diabetes and fat: Science is inaccurately represented or summarized

Dietary fiber and whole grains: Conclusions do not reflect the quantity and/or quality of science

Salt: Recommendations do not reflect limitations and uncertainties of the science

You get the idea. Within each topic, the authors point out the many flaws in the scientific “evidence” cited to support the 2010 Dietary Guidelines … the cherry-picking, the incorrect conclusions, and the contradictions. If you’re interested in the details, you can read the full paper.

Carb restriction - fat ingestion doesn't stop adaptive response to fasting

My Carb Sane-Asylum: Carbohydrate restriction regulates the adaptive response to fasting
CarbSane said... 
What the lipidstudy did was to see if adding nutrition in the form of fats modified the adaptation (e.g. just the body sensing calories). It didn't. An amino acid only infusion would be another interesting study to have done.
....when I say LC puts you in "starvation mode" it is because all of the adaptive mechanisms that kick in during longer fasts are the very same ones that do with severe carb restriction. Increased NEFA (fat mobilization), insulin resistance, ketones enhanced, gluconeogenesis and glyceroneogenesis enhanced, de novo lipogenesis decreased.

Fatty acids & ketones inhibit B-cell functions in human pancreas

My Carb Sane-Asylum: Long term exposure to fatty acids and ketones inhibits B-cell functions in human pancreatic islets of Langerhans

This underlines that high levels of both -- glucose/carbs and fatty acids -- wreak havoc on the body.

The effects of ketones were tested by 48-h exposure to β-hydroxybutyrate (β-D-OHB). Ten millimoles of D-β-OHB per L inbibited the subsequently tested insulin response to 27 mmol/L glucose by 56% (P<0.001). Half-maximal inhibitory effects of D-β-OHB on insulin secretion and insulin content were seen at concentrations between 0.5-2.5 mmol/l. Inhibition by D-β-OHB was partially reversed by etomoxir, whereas exposure to D-β-OHB failed to affect PDH and PDH kinase activities.

We conclude that fatty acids as well as ketone bodies diminish B-cell responsiveness to glucose in human islets by way of a glucose-fatty acid cycle. Increased plasma concentrations of fatty acids and ketones are likely to be important factors behind the negative influences on B-cell function exerted by a diabetic state in botb type 1 and type 2 diabetes.

How To Avoid Being Baffled By (nutrition science) Baloney - GNOLLS.ORG

You Can’t Debunk Everything: How To Avoid Being Baffled By Baloney - GNOLLS.ORG

How To Avoid Being Baffled By Baloney

Caution: contains SCIENCE!

Anyone who makes a serious effort to understand the science behind nutrition will understand immediately that news items—most of which simply reprint the press release—are usually pure baloney. In order to learn anything interesting, we require access to the papers themselves.

Unfortunately, that’s not the end of the shenanigans. Abstracts and conclusions often misrepresent the data. Data is selectively reported to omit negatives (for example, statin trials trumpet a decrease in heart disease while intentionally failing to report all-cause mortality). And experiments are often designed in such a way as to guarantee the desired result.

Is there any way to deal rationally with the unending onslaught?


Eskimo study - high omega-3 reduces obesity-related disease risk

Eskimo study suggests high consumption of omega-3s in fish-rich diet reduces obesity-related disease risk

Eskimo Study Suggests High Consumption of Omega-3s in Fish-Rich Diet Reduces Obesity-Related Disease Risk

ScienceDaily (Mar. 25, 2011) — A study of Yup'ik Eskimos in Alaska, who on average consume 20 times more omega-3 fats from fish than people in the lower 48 states, suggests that a high intake of these fats helps prevent obesity-related chronic diseases such as diabetes and heart disease.
The study, led by researchers at Fred Hutchinson Cancer Research Center and conducted in collaboration with the Center for Alaska Native Health Research at the University of Alaska-Fairbanks, was published online March 23 in the European Journal of Clinical Nutrition.

"Because Yup'ik Eskimos have a traditional diet that includes large amounts of fatty fish and have a prevalence of overweight or obesity that is similar to that of the general U.S. population, this offered a unique opportunity to study whether omega-3 fats change the association between obesity and chronic disease risk," said lead author Zeina Makhoul, Ph.D., a postdoctoral researcher in the Cancer Prevention Program of the Public Health Sciences Division at the Hutchinson Center.

Arthritis & psoriasis medications - reduced diabetes risk

Common rheumatoid arthritis and psoriasis medications are associated with reduced diabetes risk

Common Rheumatoid Arthritis and Psoriasis Medications Are Associated With Reduced Diabetes Risk

ScienceDaily (June 22, 2011) — Individuals with systemic inflammatory conditions, such as rheumatoid arthritis (RA) and psoriasis, experience a 1.5 to 2-fold increased rate of cardiovascular disease. Previous research suggests that inflammation and insulin resistance, linked with these conditions, likely accelerate the development of cardiovascular risk and diabetes. Researchers at Brigham and Women's Hospital (BWH) sought to determine whether commonly used disease-modifying antirheumatic drugs (DMARDs), which are directed against inflammation, might reduce the risk for developing diabetes in patients with RA or psoriasis.

They found that among patients with RA or psoriasis, the risk for developing diabetes was lower for those patients who started TNF inhibitor or hydroxychloroquine.

Their findings are published in the June 22/29, 2011 issue of the Journal of the American Medical Association.


PUFA & Ray Peat-ism - doubts expressed

180 Degree Health: Ray Peat - PUFA

from comments section to the above linked post:

EFA deficiency, immune function - study audit on Ray Peat position

180 Degree Health: Ray Peat - PUFA

Colldén said...
john Do you know of any studies that actually manage to induce clinical symptoms of EFA deficiency in humans (ie dermatitis etc)? I've only seen one, conducted in infants who received a completely fat-free diet, and very few studies seem to actually investigate whether the symptoms could rather be due to depletion of some nutrient due to the increased metabolism. I went through some of the literature on EFA-deficient mice, and its really true as Peat says that EFA-deficiency seems to be highly protective against many different toxins and auto-immune diseases. There's half a dozen papers on how EFA-deficienct mice are immune against streptozotocin and cyclosporin-induced diabetes, EFA-deficiency prevents autoimmune diabetes, toxin-induced renal failure and autoimmune kidney disease, makes mice strongly resistant to endotoxic shock, infectious disease and almost completely eliminates the edema associated with arthritis. Seeing as how the main purported role of PUFAs is to modulate the immune system, if they were truly essential, it just seems very odd to me that EFA-deficient animals actually show many signs of having superior immune function. Some refs: Diabetes http://www.ncbi.nlm.nih.gov/pubmed/3045812 http://www.ncbi.nlm.nih.gov/pubmed/7667243 http://www.ncbi.nlm.nih.gov/pubmed/9389417 http://www.ncbi.nlm.nih.gov/pubmed/7579534 http://www.ncbi.nlm.nih.gov/pubmed/2307932 Arthritis http://www.ncbi.nlm.nih.gov/pubmed/2307932 Endotoxic shock http://www.ncbi.nlm.nih.gov/pubmed/394879 Kidney disease http://www.ncbi.nlm.nih.gov/pubmed/2212002 http://www.ncbi.nlm.nih.gov/pubmed/2809195 Trypanosoma infection http://www.ncbi.nlm.nih.gov/pubmed/1342611 Antimicrobial activity http://www.ncbi.nlm.nih.gov/pubmed/2649598 http://www.ncbi.nlm.nih.gov/pubmed/9119445

Sugar vs. Starch - Matt Stone explains Ray Peat

180 Degree Health: Ray Peat - Sugar vs. Starch

I didn’t want to give up on the Ray Peat topic altogether now. There is still a lot to be said. In fact, his lengthy article titled “Glycemia, Starch, and Sugar in context” is a perfect article to deconstruct. It is full of many of Peat’s main philosophies about stress hormones, blood sugar regulation, metabolism, gelatin, polyunsaturated fat – you name it. It’s all there in that article. And it’s the perfect article to examine because some of it is great, and some of it is downright silly. It’s a great blend. In fact, it will probably take many posts to break this single article down – but once we are through most of you will have a pretty good idea about Ray Peat, and also will be left, hopefully, with a balanced view of him as a researcher (which is something few can claim – most either think he is a total wacko or is like the Messiah of nutrition).

I will not put every paragraph in the article under the microscope, but we will start with a few that I have selected to discuss and keep the conversation going for a while. In so doing, hopefully we’ll get somewhere. Begin! (spoken in the tone of the original Mortal Kombat video game).

“Judging by present and past statements of the American Dietetic Association, I think some kind of institutional brain defect might account for their recommendations. Although the dietetic association now feebly acknowledges that sugars don't raise the blood sugar more quickly than starches do, they can't get away from their absurd old recommendations, which were never scientifically justified: “Eat more starches, such as bread, cereal, and starchy vegetables--6 servings a day or more. Start the day with cold (dry) cereal with nonfat/skim milk or a bagel with one teaspoon of jelly/jam. Put starch center stage--pasta with tomato sauce, baked potato with chili, rice and stir-fried beef and vegetables. Add cooked black beans, corn, or garbanzo beans (chickpeas) to salads or casseroles.”

Peat, in his disdain for mainstream nutrition beliefs, is poking fun at the dietary recommendation to base the diet primarily around starches and not simple sugars. Of course, these recommendations were based on widely held but later discovered-to-be-mistaken beliefs that complex carbohydrates – like grains, potatoes, corn, and beans, digested more slowly than simple sugars comprised of less “complex” molecules. It had been known for ages that these foods generally led to more stable blood glucose levels (measured over a 6-hour time period as opposed to just basing everything off of what happens in the first half hour), and were great preventatives against hypoglycemia unlike the foods listed by early anti-sugar author E.M. Abrahamson (1951) who gave the following prescription for those prone to hypoglycemia, “no sugar, candy, or other sweets, no cake with icing, no pies or other pastry, no ice cream, no honey, no syrup, no grape juice or prune juice. And regrettably, our string of ‘no’s’ includes cocktails, wines, cordials, and beer. Finally, if you have hyperinsulinism, you must avoid caffeine as you would the pest.”

Of course, there are many diseases including hereditary fructose intolerance and various glycogen storage diseases in which starch is a completely safe food to eat, but the ingestion of any of the foods listed by Abrahamson containing simple sugars can cause life-threatening bouts of hypoglycemia. This has nothing to do with the absorption rate of the carbohydrates, and in my experience the absorption rate of the carbohydrates has nothing to do with a food’s ability to trigger hypoglycemia. Quite simply, absorption rate or “glycemic index” of foods or the insulin spike after eating rapidly-absorbed starches has nothing to do with hypoglycemia. Thinking that it does is just another pseudoscientific sasquatch.

Thinking that such recommendations were made due to some brain defect is even more offensive, as many of the mantras of mainstream nutrition are based on the pioneering work of Denis Burkitt, Hugh Trowell, T.L. Cleave, and others who spent time in Africa gathering hard data on the rates, or absence I should say, of many cancers, heart disease, diabetes, obesity, constipation, hemorrhoids, varicose veins, appendicitis, diverticulosis, and many others on diets built around starchy agricultural staples – notably whole grains, corn, root vegetables, and the like. It’s not like these beliefs were pulled out of thin air as part of some government propaganda machine. And as Burkitt witnessed, the more food that was displaced with whole grains and tubers, the lower the fasting glucose level of the population.

"The Dietetic Association's association with General Mills, the breakfast cereal empire, (and Kellog, Nabisco, and many other food industry giants) might have something to do with their starchy opinions. Starch-grain embolisms can cause brain damage, but major money can also make people say stupid things."

These food companies make more money the more high-fructose corn syrup and vegetable oil they manage to squeeze into the food, as these are generally much cheaper calories than those in villainous grains or potatoes (although they are still plenty cheap). More importantly, the more fat and extra sweet HFCS in the product, the more of it consumers buy and eat because sugar – particularly high-fructose corn syrup because it is sweeter, and fat, are more stimulating than starch, generally-speaking (although there are plenty of people that get more riled up about chips, Cheez-its, and baguettes than sugar-laden sweets). To think that such companies are behind some massive scheme to steer people towards vile corn and potatoes and away from wholesome simple sugar is comical to put it lightly.

"In an old experiment, a rat was tube-fed ten grams of corn-starch paste, and then anesthetized. Ten minutes after the massive tube feeding, the professor told the students to find how far the starch had moved along the alimentary canal. No trace of the white paste could be found, demonstrating the speed with which starch can be digested and absorbed. The very rapid rise of blood sugar stimulates massive release of insulin, and rapidly converts much of the carbohydrate into fat."

I smell more sasquatch here. In fact, the smell is so strong the John Lithgow is outside my window shouting the name “Harry” over and over. Jack Black and Kyle Gass are here with a bottle of aerosol Trap B Gone and are setting up a drumset as we speak. Sasquatch’s “drumming is kickass” they tell me.

Insulin converting carbohydrate into fat? That’s not how insulin works at all. In fact, a solid debunking took place a couple months back at http://www.carbsanity.blogspot.com/ in which it was shown that the body is in negative fat balance (burning more fat than storing) during postprandial insulin spikes – like the kind you get after having some good old corn starch. On top of that, the easiest carbohydrate to convert to fat has been shown time and time and time and time and time again to be the one that travels to the liver and is digested most slowly. It’s called fructose. Not only does the presence of fat make fat storage easier, if fructose is converted to fat in the liver (which it can be under certain circumstances) it increases insulin resistance, which can lead to increased fat storage (insulin lowers appetite and increases metabolic rate, so becoming unresponsive to the hormone has a tendency to increase appetite and reduce metabolic rate).

Insulin is also intricately tied to leptin, the master hormone of managing the calories in/calories out equation. Surges in insulin cause surges in leptin, which lowers appetite and increases the metabolic rate. Stating that making insulin rise leads to becoming fat is a complete misrepresentation of the bigger picture. In fact, starch-based diets usually lower appetite dramatically, and many starchy foods like potatoes and oats are known to satisfy the appetite on fewer calories than just about any foods known (higher “satiety index”).

Speaking of corn starch specifically, this has actually been used successfully by Francine Kauffman of the American Diabetes Association in the prevention of early morning hypoglycemia in diabetics – more evidence that absorption rate is not the prime determinant of whether or not a particular carbohydrate goes on to trigger hypoglycemia and general blood glucose dysregulation.

Anyway, don’t get the wrong idea here. I’ve been eating simple sugars in favor of starches myself for many months now and have noticed some apparent benefits. Many seem to do better with sugars than starches for keeping hands and feet warm, producing more energy, getting better sleep – probably due to enhanced liver glycogen storage, and so forth. Many fare better from a digestive standpoint on fruit, juice, and sugar than more complex carbohydrate molecules. Some even report a lowering of appetite on sugar vs. starches, especially with the consumption of whole fruits which, like most starchy staples, are very high satiety index foods. Fruit is also generally more nutritious and hypoallergenic.

So be open to either, or a combination of the two. It’s up to everyone to experiment for themselves to see what the relative benefits and drawbacks of the two basic types of carbohydrates are. But the point here is to shoot down Peat’s wacky and erroneous biochemical justification of the outright superiority of sugar over starch. There is not a clear cut right or wrong carbohydrate, and the mainstream belief that “complex” carbohydrates are superior to simple sugars is not the result of a governmental or agribusiness conspiracy.

In the next episode, we will continue looking closer at Ray’s cookie-cutter and false portrayal of insulin as being a hormone that, if driven up, will drive blood sugar down and cause hypoglycemia. Don’t worry, Ray’s got some tremendous gems in this article as well, as he is one of the few that actually does have some understanding of type 2 diabetes, realizes that it is a shortage, not a surplus of glucose at the cellular level, and so on.

For more discussion on the sugar and starch issue, read this free book on how to raise your metabolism.

Low carb blogs - more accepting starch now?

from comments on this article: 180 Degree Health: Ray Peat - PUFA
Wolfstriked said... 
Hey Matt and crew.Lately I have stumbled upon two things that have brought alot of happiness to my life in the form of fatloss,sex drive,mood and energy.I wanna post this here because it has alot to do with Matt's strong stance on the "carb wars" and how we might be wrong in trying to drop carbs from our diets.Just look at all the low carb sites that are slowly saying its ok to eat rice and potatoes and now fruit.They claim LC but slowly the amounts will start to come back up to SAD levels. I have nothing against LC....just need to point that out.Its just that I have a hard time believing that all the doctors and LC gurus seem to be oblivious of Japan and the known health of its people.They eat rice of god forbid wheat(noodles)at every meal.The starch is main component with toppings like eggs,fish and meat with some vegetables.WHY WHY is this not mentioned....instead all I hear is that the Japanese eat vegetables and raw fish when a staple served in their homes is beef and potato stewed in soysauce or noodles with pork and veggies in soup. I also have found that in Japan its common thought that to lose weight you just cut the fat.....OMG!! So recently I have decided upon following the Japanese style diet just Americanized for some meals.I am talking bagels and 3 hard boiled eggs with cup of joe for breakfast from local NYC cart.Lunch and dinner is typically a starch and some meat and veg Japan style in that I top with soy sauce usually.I tried cutting the protein rich foods out two days ago but found I started getting pains in my liver(why is that)and it went away when I put back in the meat. Weightloss is superb of course due to it being low calorie meals.I know it goes against the high amount of food you push to drive metabolism but I believe now that one needs to do high and low calorie wise for best health.Its in tune with your recent posts on intuitive eating. See I always seem to do well on low calorie and then 3 days in my body rejects and I bloat out.So I am starting to notice that if I eat an extra HED style meal(butter,rice,meat) that day,I wake up with looser fitting pants.Could be why skinny people stay skinny...they eat intuitively and feast.Then the appetite is regulated from the feast the day before for a day or two after at which point....for me at least I bloat and appetite goes thru the roof.This is new to me and today I have eaten only 1000cal and not really hungry attributed to the feast 2200cal from yesterday
In case my point did not get thru well.I believe now that the best tool in the war against fatloss is to....first cut calories to lose fat...then to eat extra when you feel the diet stops working. I tried the Leangains diet a few months back and found fatloss was superb and muscle growth also but hate any diet based on meat.  I now think that LeanGains is working(fatloss wise)due mainly to the fat that you double calories on days you WO.....not that you intermittant fast or that its very high protein(the high protein does pack on the muscle though if thats what you want)but that you alternate low calorie days with high calorie which prevents the slowdown of metabolism.I find that I have to take a dump and feel hot and sweaty a 1/2 hour after this large meal.

Matt Stone - Dr Kurt Harris critiques

Archevore - Archevore Blog - 180 + 180 = 360

180 + 180 = 360

Reader Jeff writes in with a comment about Matt Stone of 180 Health.

Matt is the subtle attention-shy guy who poses shirtless holding a pig’s head on his blog.
Matt doesn’t really need any attention from me, he is busy commenting in a “contrarian” fashion all over the blogosphere right now. However, enough readers are asking me what I think that I should say something, I suppose.

Jeff writes regarding Matt Stone's guest post on Tom Naughton's blog re colton osborn's question- i just went over and read the post at the link. i think the key section is:
And therein lies the true danger of uber-low-carbohydrate diets. All my experience tells me that, the first few years aside, a low-carbohydrate diet and certainly a full-blown ketogenic diet exacerbates a low metabolism. It is not a matter of having a genetically-doomed dysfunctional thyroid gland; it is fixable, and it lies at the core of the health problems we’ve seen explode over the last century. This is why all prolonged restricted diets, low-carb included, in the words of Robert Atkins himself (from page 303 of Dr. Atkins’ New Diet Revolution):
“…tend to shut down thyroid function. This is usually not a problem with the thyroid gland but with the liver, which fails to convert T4 into the more active thyroid principle, T3. The diagnosis is made on clinical grounds with the presence of fatigue, sluggishness, dry skin, coarse or falling hair, an elevation in cholesterol, or a low body temperature.”
To that I will add constipation, bad moods, heartburn, cold hands and feet, and a whole host of other minor but significant health problems. To get an idea of how “shutting down the thyroid” can manifest, Mark Starr’s chapter on Hypothyroidism symptoms is 83 pages long.
Jeff here- most of what is in the post is fully compatible with PaNu. But Matt Stone asserts that once you've been on zero carb or very low carb for a while [several years] you'll run into problems as specified above. The carbs he recommends sound like potatoes and rice, not clear what he thinks about whole grains, but the bottom line question seems to be about thyroid function over the long term.  I read the post and it starts out reasonably. Matt's hyping a pseudo -contrarian position that has some truth to it, but reading him later he goes off the rails when he starts talking about cortisol and thyroid function.

His first target is really a straw man. PaNu, Wholehealthsource and Peter at Hyperlipid all target fructose and linoleic acid as the main causes of metabolic disturbance in the western diet. Even Gary Taubes in his recent lectures has said "it may indeed all be fructose". None of us, read carefully, claims that "carbohydrates = disease".

His observation that some people may not feel good, even "hypometabolic" on VLC I don't take issue with. It seems like common sense that you might feel better eating more or less of just about anything. As long as you are avoiding the neolithic agents, tinker away! (That's for Brett and Nassim)
My blog with 60 or so main posts and pushing 3000 comments does not have any content from me prescribing precise ratios of anything, except for when advising how to lose weight. I respect the Optimal diet and Peter but I think any tightly defined macro ratio is rather artificial, including Kwasniewski's. I am sure that bias shows in my irritation at the bodybuilding questions : )

At the same time, Stone's statement that long term ketogenic eating per se ruins your metabolism is much less supportable than the "all carbs are metabolic poison" straw man he is attacking. Again, even Taubes does not really say this in GCBC.

My own view on the ratio of carbs in the diet should be pretty clear by now.

1) I think a wide range is tolerable for those with normal metabolism. For those about to ask "how wide" - OK, let's say 5% to 40% or even more if you can tolerate it and the rest of your food is very high quality. If your metabolism is damaged (you know who you are - type II or obesity prone) or you don't tolerate starches well like me, you should probably stay on the low end of carb intake. 

2) I think the paleolithic principle itself argues against LC and VLC being damaging the same way it argues against plants and all carbs as being poison. It just makes no sense, as it implies that humans in any given econiche, even one rich in a huge variety of animal foods, would have been at risk of metabolic damage from being in long term mild ketosis if they were not able to find enough starchy tubers and fruit in season. (We've agreed that grains like white rice are a recent food, I hope).
Enough nonstarchy greens to choke a gorilla with an otherwise all animal diet will not keep you totally out of ketosis, I guarantee. If it did, I wouldn't want to share your bathroom.
Of course, you can start eating a lot of coconuts like the Tokelauans or Kitavans and you can elevate your B-hydroxybutyrate even with a normal carb intake. Uh-oh - now our thyroid glands will die!

3) I suppose it is a corollary of my own paleo principle that I don't like approaches that require "seeking" behavior for something that provides only calories. "I'd better eat some carbs or my thyroid and adrenal glands will be screwed up". Really? HGs had to consciously think about whether they were getting enough starch? Or is starch just something that we eat because it helps us not starve? 

4) On the other hand, avoidance behavior is totally compatible with the paleolithic principle. "Avoid that, as it is outside of our evolutionary experience or causes metabolic effects that are outside our experience in the amounts that are available". This is my template. Fructose, wheat and excess linoleic acid.

5) It is true that being in negative energy balance – losing weight -generates an energy conserving response. That is not surprising. Once you are at equilibrium though, does a lower free T3 with normal TSH and T4 on lower carbs mean something pathologic? What if you had cold hands and a low basal temperature when even you ate 50% of calories as carbs? Are you now supposed to go from 10% to 70% to "restart your thyroid" or are you rather still hypothyroid because you have always been hypothyroid and you are just no longer euphoric now that you have stopped losing weight? Remembering your mood or body sensations one hour ago is hard enough. We are supposed to remember what they were years ago?

6) In answer to the idea that we need to carefully regulate macronutrient ratios to control the function of our thyroid and adrenal glands I have only one comment for now:
Lacks biological and evolutionary plausibility.

To summarize, Matt is a clever and entertaining writer, but his main target is a straw man, as most of the science oriented paleonutrition blogs are not really "low carb" blogs at all. His observation that starch per se need not be unhealthy is not really that controversial.

Matt's claims about his own serum BG after meals should be published as a case report in a medical journal. They are at odds with clinical studies I have read on glucose metabolism in normal highly insulin sensitive young people (can you say "superhuman"?).

Matt's got some good observations, but is over or mis-interpreting the literature in the realm of endocrinology. I did not notice if he has any medical or scientific credentials, but his views of hormonal action lack nuance, to say the least. He is also avidly mining the "I feel like shite, it must be my thyroid or adrenal glands" meme.

Matt Stone - Paleo Hacks critic

Low-Carb Paleo Eating Ruined Matt Stone's Health? - Paleo Hacks.com

After finding low-carb paleo diet to be perfect for me and my lifestyle I am so dissapointed to hear Matt Stone at 180-degree health refute what I beleive. Stone use to be low-carb paleo and suffered several health problems and talks about his client with the lowest body temperature being a guy after he went LC paleo. I understand people gaining weight after stopping LC paleo bc I beleive they shouldnt be eating foods that aren't LC paleo. But Stone says LC paleo ruins metabolisms. What do you think?



He has no qualifications. He is the glenn beck of paleo/health blogs

Glycemia, starch, & sugar in context - by Ray Peat Ph.D

Glycemia, starch, and sugar in context


Glycemia, starch, and sugar in context


Monosaccharide -- a simple sugar; examples, glucose, fructose, ribose, galactose (galactose is also called cerebrose, brain sugar).
Disaccharide -- two monosaccharides bound together; examples, sucrose, lactose, maltose.
Oligosaccharide -- a short chain of monosaccharides, including disaccharides and slightly longer chains.
Polysaccharide -- example, starch, cellulose, glycogen.
Glycation -- the attachment of a sugar to a protein.
Lipolysis - the liberation of free fatty acids from triglycerides, the neutral form in which fats are stored, bound to glycerine.
In the 1920s, “diabetes” was thought to be a disease of insulin deficiency. Eventually, measurements of insulin showed that “diabetics” often had normal amounts of insulin, or above-normal amounts. There are now “two kinds of diabetes,” with suggestions that “the disease” will soon be further subdivided.
The degenerative diseases that are associated with hyperglycemia and commonly called diabetes, are only indirectly related to insulin, and as an approach to understanding or treating diabetes, the “glycemic index” of foods is useless. Physiologically, it has no constructive use, and very little meaning.

PUFA essential nutrient, or toxic? - by Ray Peat Phd

Unsaturated fatty acids: Nutritionally essential, or toxic?

by Ray Peat Phd

Unsaturated fatty acids: Nutritionally essential, or toxic?

In 1929 George and Mildred Burr published a paper claiming that unsaturated fats, and specifically linoleic acid, were essential to prevent a particular disease involving dandruff, dermatitis, slowed growth, sterility, and fatal kidney degeneration.

In 1929, most of the B vitamins and essential trace minerals were unknown to nutritionists. The symptoms the Burrs saw are easily produced by deficiencies of the vitamins and minerals that they didn't know about.
What really happens to animals when the "essential fatty acids" are lacking, in an otherwise adequate diet?

The Secret to Long Life? HA Hyaluronic Acid

Uploaded by on May 20, 2009
Japanese researchers believe that the secret to a healthy and long life could be a substance called Hyaluronic Acid.
Find out more at www.coralsupreme.com

Omega-6 & 3 Consumption over the Last Century

Whole Health Source: US Omega-6 and Omega-3 Fat Consumption over the Last Century

by Whole Health Source

US Omega-6 and Omega-3 Fat Consumption over the Last Century

Omega-6 and omega-3 polyunsaturated fats (PUFA) are essential nutrients that play many important roles in the body. They are highly bioactive, and so any deviation from ancestral intake norms should probably be viewed with suspicion. I've expressed my opinion many times on this blog that omega-6 consumption is currently too high due to our high intake of refined seed oils (corn, soybean, sunflower, etc.) in industrial nations. Although it's clear that the quantity of omega-6 and omega-3 polyunsaturated fat have changed over the last century, no one had ever published a paper that attempted to systematically quantify it until last month (1).

Drs. Chris Ramsden and Joseph Hibbeln worked on this paper (the first author was Dr. Tanya Blasbalg and the senior author was Dr. Robert Rawlings)-- they were the first and second authors of a different review article I reviewed recently (2). Their new paper is a great reference that I'm sure I'll cite many times. I'm going to briefly review it and highlight a few key points.

1. The intake of omega-6 linoleic acid has increased quite a bit since 1909. It would have been roughly 2.3% of calories in 1909, while in 1999 it was 7.2%. That represents an increase of 213%. Linoleic acid is the form of omega-6 that predominates in seed oils.

2. The intake of omega-3 alpha-linolenic acid has also increased, for reasons that I'll explain below. It changed from 0.35% of calories to 0.72%, an increase of 109%.

3. The intake of long-chain omega-6 and omega-3 fats have decreased. These are the highly bioactive fats for which linoleic acid and alpha-linolenic acid are precursors. Arachidonic acid, DHA, DPA and EPA intakes have declined. This mostly has to do with changing husbandry practices and the replacement of animal fats with seed oils in the diet.

4. The ratio of omega-6 to omega-3 fats has increased. There is still quite a bit of debate over whether the ratios matter, or simply the absolute amount of each. I maintain that there is enough evidence from highly controlled animal studies and the basic biochemistry of PUFAs to tentatively conclude that the ratio is important. At a minimum, we know that excess linoleic acid inhibits omega-3 metabolism (3, 4, 5, 6). The omega-6:3 ratio increased from 5.4:1 to 9.6:1 between 1909 and 2009, a 78% increase.

5. The biggest factor in both linoleic acid and alpha-linolenic acid intake changes was the astonishing rise in soybean oil consumption. Soybean oil consumption increased from virtually nothing to 7.4% of total calories, eclipsing all sources of calories besides sugar, dairy and grains! That's because processed food is stuffed with it. It's essentially a byproduct of defatted soybean meal-- the second most important animal feed after corn. Check out this graph from the paper:

I think this paper is an important piece of the puzzle as we try to figure out what happened to nutrition and health in the US over the last century.

Omega 6 & 3 in nuts, oils etc - harm from too much

Omega 6 and 3 in nuts, oils, meat and fish. Tools to get it right. | Julianne's Paleo & Zone Nutrition Blog

Omega 6 and 3 in nuts, oils, meat and fish. Tools to get it right.

You are strict paleo, you eat nothing but meat, seafood, fruit and veggies, nuts and seeds. Your snacks are mainly a handful of almonds. Did you know just 60 grams of almonds gives you all the omega 6 you need – and more may be detrimental?

One of the ways our diets have changed dramatically from the diets of our ancestors and even the very recent past is the ratio of Omega 6 to Omega 3 polyunsaturated fatty acids in the food we eat. A huge amount has been written about this subject, dozens of studies have been published. I’m not going into detail, the object here is to provide tools to help you get this balance right. At the end of the page – I’ve posted some links to other interesting blog posts and articles.