Does Sugar make you Fat?

Technically sugar is not the direct cause of obesity.  The most fattening or obesigenic foods are those that combine carbohydrate with fat.  Think potato chips.  A potato chip delivers a load of starch and fat.  The highly processed potato starch is high-glycemic meaning that it is rapidly absorbed and converted into blood glucose.  Your body responds by releasing a lot of insulin.

The combination of high insulin and lipids levels in the blood causes an enhanced uptake of fat storage in your fat cells. 

High glycemic carbohydrates raise blood insulin levels much higher than an equivalent amount of glucose from a high fiber low glycemic carbohydrate.  Most of the absorption is in the upper small intestine, so the release of hunger suppressing hormones in the lower small intestine is muted meaning that more food is required to satisfy that hunger. 

So, eating potato chips spikes blood insulin and concurrently raises blood lipids which the body then stores as fat at an accelerated pace. You eat more because it doesn’t satisfy so much.  The high insulin leads to a sharp drop in blood glucose a few hours later making you want to eat more. 

This is why processed foods which lack fiber are fattening.

But what about Sugar?  Sugar enhances the process driving fat accumulation.  Sugar catalyzes the process by making you insulin resistant leading to even higher blood insulin levels. 

Eating the high amount of sugar commonly found in processed food floods the liver with fructose where a significant amount gets converted directly to liver fat.  High liver fat makes the liver insulin resistant.  The same fat gets released in the blood as triglycerides and contain the type of fat that causes visceral fat accumulation. Visceral fat is associated with insulin resistance.  The mechanism for all that is unclear.  Are visceral fat and insulin resistance both effects?  Or does visceral fat cause insulin resistance?

But I think we have enough to know that high sugar consumption causes high insulin and leads to insulin resistance as assuredly as high consumption of drugs leads to resistance to the effects of those drugs. 

So, sugar makes you fat indirectly.  It’s like high winds spreading a wild fire.

A positive trend in America is that per capital sugar consumption is going down. That trend leads some to believe that Sugar does not make you fat since sugar consumption is down but obesity rates keep rising. Don’t be mislead by that claim.  Per capita sugar consumption still remains high.  A modest reduction in sugar consumption will not reverse obesity already acquired.  Continued high sugar consumption is still associated with continued increases in obesity rates.  But the rate of increase in obesity could slow a bit. It appears that it has.  The data supports the theory that sugar does in fact make you fat.

Dr. Sebi

My wife asked me to research a Dr. Sebi.  She is thinking of reading a book about his health and diet recommendations.  (Actually, it is an audiobook, Seven Days In Usha Village, A Conversation with Dr. Sebi.)

He’s certainly an interesting character.  But first, my initial reaction to him and his teachings are best summarized by my esteemed friends who live in nearby Heritage Park as expressed here.

For a closer look, I found a favorable or at least neutral website article with a lot of information on him including an hour and a half video by “Dr.” Sebi.  I put “Dr.” in quotes because it appears he has no academic training of any kind whatsoever.   More information regarding his life and work may be found at Quackwatch.  Note that “Dr.” Sebi is no longer with us having died in a Guatemala in jail pending charges of money laundering in 2016.

He rejects modern medicine pretty much in its entirety, including the germ theory of disease, attributing virtually all sickness to “mucous” or due to the body’s mucous membrane being compromised.  His dietary recommendations amount to a restricted form of a vegan whole and raw food diet.  The restriction part is that all of the foods he recommends are “alkaline” rather than “acidic”.  He claims to be able to cure virtually any sickness including diabetes, cancer, and aids by dietary changes and by the use of herbal medicine which may be obtained for a substantial purchase from his website.

I plan on examining a number of different diets and their benefits and drawbacks.  The best advocate I have seen thus far for a raw food vegan diet is Andrew Perlot (see Why You Feel Happier On A Raw Food Diet.)  He subsisted on a purely raw food vegan diet for 11 years, but in 2016 he introduced some cooked foods to increase his protein intake.  Nevertheless, his diet is substantially a raw food one even now.

I think there is no doubt that some have benefited from a raw food vegan diet, especially for specific conditions such as the colitis that affected Andrew Perlot.  People will likely lose substantial weight on such a diet and that by itself could cure Type II diabetes in some people. Diabetes, however, is a complicated condition, and I don’t believe there is any one diet or approach that will cure Type II diabetes in all cases.  More on that another day.

Note that the only evidence “Dr.” Sebi offers as support for his prescriptions is anecdotal evidence — i.e. testimonials.  Anecdotal evidence is nearly worthless as a form of evidence.  If anecdotes consisting of personal testimonies accumulate, then that may suggest avenues of research or a source of hypotheses for testing, but that is all they are good for.  Anecdotes or testimonies that are accumulated and presented as evidence to advocate for a particular idea–well that is simply cherry picking and is logically fallacious.  I’m afraid I have to concur with my Heritage Park friends regarding “Dr.” Sebi.

 

 

 

The Hall experiment.

In July 2016, the American Journal of Clinical Nutrition published a study that claimed to falsify or refute the “carbohydrate-insulin hypothesis” for obesity.  This is a theory promoted by Dr. Jason Fung and others who criticize diets high in sugar and carbohydrates as promoting high insulin blood levels.  The high blood insulin, in turn, suppresses the body’s ability to release and burn fat and instead drives fat into fat cells making a person fatter.  Further claims include the idea that a person’s basic metabolic rate will slow in the presence of these elevated insulin levels (Hyperinsulinemia).

The study was funded by the Nutritional Science Initiative, an organization founded with the help of Gary Taubes, an advocate of the carbohydrate-insulin hypothesis.  The lead scientist of the study, Dr. Kevin Hall, explains his work in this interview.

Obviously, Jason Fung doesn’t agree.  He responds in Here’s $5, Kevin Hall, go buy yourself a clue.

Here is my simplified (perhaps oversimplified) explanation of what was done in the experiment:

•  The experiment was done with 17 fat men.  They were confined to a metabolic ward for two months where all of their food consumption and exercise were carefully controlled and measured.
• They were fed two diets.  For the first month, they consumed a base diet (BD) where ~25% of total calories came from sugars.  For the second month, they consumed ketogenic diet where <2% of total calories came from sugars.
• Actual energy expenditure was measured directly by having the subjects spend two days each week in an Energy Expenditure chamber. Details of how this was done are given in the paper.
• For the first two weeks on the base diet, the number of calories each person consumed was adjusted to achieve “energy balance”, meaning that they should be burning up as many calories as they eat.  After two weeks, the number of calories each subject ate each day was “clamped” at that energy balance level and was kept the same for the next two weeks of the BD and for the four weeks of the KD diet.

The results of the experiment are summed up in a set of graphs from the paper which I reproduce at the end of this post.  Here is my summary of the results:

• The subjects lost weight, including fat during the last two weeks of the BD diet when they were supposed to be in energy balance. This is called “surprising” in the study.
• Once the subjects switched to the KD diet, their weight dropped faster for a few days, then leveled off to a flat or much slower weight loss.
• During the first two weeks of the KD diet, the rate of reduction in body fat actually went down. For the last two weeks of the KD diet, the rate of reduction of body fat went back up to about the same rate as in the last two weeks of the BD.
• The subjects base energy consumption went up rapidly in the first week of the KD diet, then lowered from that higher level over the course of the three weeks. The net increase in base metabolism was barely significant according to the statistical analysis.
• The daily insulin secretion rapidly and persistently decreased by 47% after the introduction of the KD and total urinary ketone excretion increased >10-fold. These confirm that the patients were in ketosis on the KD diet.

My summary of the conclusions of the study is as follows.  I use quotes from the article:

•  The carbohydrate–insulin model predicts a greater rate of body fat loss during the KD period. Our data do not support this prediction.
• The carbohydrate–insulin model predicts that the KD would lead to increased EE, thereby resulting in a metabolic advantage amounting to ~300–600 kcal/d (21, 22). Our data do not support EE increases of that magnitude.
• Mathematical model simulations predicted that cutting dietary carbohydrates to very low amounts would reverse this trend [high carbohydrates causing a decrease in EE) and lead to slightly increased EE. This prediction appears to have been borne out in our data.
• In summary, we found that a carefully controlled isocaloric KD coincided with small increases in EE that waned over time. Despite rapid, substantial, and persistent reductions in daily insulin secretion and RQ after introducing the KD, we observed a slowing of body fat loss. Therefore, our data do not support the carbohydrate–insulin model predictions of physiologically relevant increases in EE or greater body fat loss in response to an isocaloric KD.

What should we think of this study?  Here are Dr. Fung’s criticisms as I understand him.

First, Fung points out a weakness in the study. He says, “When patients embarked on their run in phase, they were switched to a 2700 calorie/day high sugar high carb diet, meant to replicate the Standard American Diet (SAD) . . . nobody believes it should cause fat loss. But it did. Why?”

Fung explains this as a common effect of this kind of experiment, “Anybody who has done research knows why. It’s the effect of going into a study and knowing that people are testing you. It’s a universal effect.”

To my surprise, the authors of the paper admit this is true! In the discussion portion, they say, “A major limitation of our study is the unintentional weight loss. Despite slight positive energy balance during the chamber days, the overall negative energy balance amounted to ~300 kcal/d and was likely due to greater spontaneous physical activity on non-chamber days. This occurred despite confining the subjects to metabolic wards and our best efforts to maintain constant activity levels by prescribing 90 min of fixed intensity stationary cycling exercise every day.”  The experiment subjects exercised more at the start to perform better for the test because they knew they were being watched.  The question is did this behavior persist during the last half of the experiment?

The paper implies that carbohydrate-insulin model prediction a greater rate of fat loss on a KD diet is false when they say their data does not support this prediction. But this conclusion is worthless if the initial fat loss on their BD is an artifact of the experiment.

Second, It also calls into question their conclusion that the carbohydrate-insulin model predicts that the KD would lead to increased EE, thereby resulting in a metabolic advantage amounting to ~300-600 calories per day. Fung points out that they did find an increase in EE of 57 calories per day that correlated with the KD with a 99.96% chance is not coincidental. Now, this 57 calorie difference is not great, but it appears to be absolute. When we speak of metabolic advantage, we have to ask compared to what? As I see it, no conclusion can be drawn regarding the magnitude of any metabolic advantage without an adequate measure of expected decreased in EE or basal metabolism from calorie-restricted diets.

And that is a gaping hole that I see in the study. The big criticism of calorie-restricted diets based on the calories-in-calories-out model concerns metabolic damage caused by these diets. Fung refers to a 2012 study spear-headed by the well known Havard nutritional researcher Dr. David Ludwig, Effects of dietary composition on energy expenditure during weight-loss maintenance.

That study compares the basal metabolic weight of subjects during the maintenance phase after wieght loss.  Fung reproduced the following graphic:

This summarizes the results of the Havard study.  After dieting, the energy expenditure of the dieters was lowered.  That is not surprising.  Overweight people in general burn more calories to maintain body heat for their larger body mass, so overall energy expenditure is expected to decrease some after wieght loss.  But notice the difference between those who lost the weight on a low fat (LF) diet versus those who lost the weight on a very low carbohydrate diet (VLC).  The difference in 325 calories per day.  That is where the metabolic advantage becomes evident.  The reason for the advantage has more to do with the harm of calorie-restricted diets than it has to do with metabolic advantages conferred by a KD.  It seems to me that this difference (this advantage) would persist even if we showed that weight maintenance on a KD did not alter EE at all.

A further issue which occurs to me concerns whether or not the obese subjects were insulin resistant.  Obese people are in fact typically insulin resistant.  Typically, insulin resistant people will maintain a much higher level of blood insulin for a longer time period following a meal.  My question is how this might affect energy expenditure.  It would be nice to see an experiment like this performed on people with normal weight and known not to be insulin resistant.

It seems to me that this experiment does cast some doubt on the carbohydrate-insulin model of obesity, but it is far from a slam-dunk, nor does it appear to come even close to refuting the efficacy and metabolic benefits of ketogenic diets versus typical calorie restricted dieting regimes that have been the mainstay of weight loss therapy for the last many decades.  Hall and company are far too confident in their assertions that the carbohydrate-insulin model has been refuted.

Nor does it call into question the mechanisms described by Dr. Robert Lustig in  Sugar, The Bitter Truth.   Elevated blood glucose accompanied by high levels of blood fat either from fatty food or from the liver where fresh triglycerides are produced from fructose is both inflammatory and puts fat production into high gear.  A sustained diet of this kind which is essentially most of the Standard American Diet (SAD) leads to obesity, diabetes and heart disease.

This blog so far

Well, I have not posted anything to this blog for a few weeks.  I’ve been busy with personal matters (I might be moving).   My last three posts were a criticism of a YouTube video by Cyrus Khambatta that allegedly refuted low-carb ketogenic diet claims.  The vacuous video (i.e free of any information backed up by any sources) was riddled with bad arguments.  I thought it worth covering to expose the bad reasoning on display.

But, I am not intending to criticize vegetarian or vegan diets or research.  There are many intelligent and interesting authorities on YouTube, ones who back up their claims with facts, available from a vegan perspective.  Among these are Dr. Michael McGreger, Dr. John McDougal, and Mic. the Vegan.  You may add to those other authorities who promoted mainly plant-based whole food diets even if they are not pure vegan such as Dr. Valter Longo.

Nevertheless, I have been experimenting with both fasting and low-carb diets because of the significant number of studies showing the efficacy of these diets for weight loss and for improving blood panel numbers (lowering triglycerides and raising HDL cholesterol).  I am not convinced at all that a ketogenic diet is an appropriate long term.  Right now, I view it as a therapeutic diet, and my use of it along with fasting has been positive.  I have lost weight and both my HDL and blood triglycerides have improved immensely (see my post Is High LDL always bad?).  My LDL was very high while fasting which is not surprising.  I expect LDL numbers to adjust lower in future testing, perhaps when I am not in ketosis.

I believe a ketogenic diet helps in many cases.  Cancer, for example.  It’s now generally recognized that cancer cells preferentially feed on glucose, and that some cancers at least can be treated using fasting or a ketogenic diet as a secondary or follow-on treatment. (see Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism.)  If I were diagnosed with cancer, I would certainly look into this as a possible additional therapy.

My first post was a long one, a diatribe against sugar.   It was based mainly on the work of  Dr. Rober Lusting.  But other sources including the work of Dr. Jason Fung and Gary Taubes.  I may cover that material again breaking it up into smaller more focused posts.  My main point in that post was that excess sugar consumption leads to obesity and diabetes mostly due to the effect it has on blood insulin levels.  This is known as the insulin or hormonal hypothesis of obesity.

I started that post with my own contribution.  A misleading graph by  Dr. Stephan J. Guyenet to discredit any inference to a cause based on the correlation between increased sugar consumption and obesity rates.  It showed that per capita sugar consumption has been going down since around 2000, but obesity continued to climb.  That supposedly made the inference of a possible causative link between the two to be less tenable.  I redrew the graph to reflect the data more accurately and pointed out what should have been obvious.  Per capita sugar consumption remains very high, and a drop in that value does not mean that obesity will decline.  People who were obese before remain obese and the number of new cases of obesity will still continue to rise albeit at a slower rate.  The graph actually shows this slowdown.  That level of correlation would suggest a stronger, not a weaker likelihood of a causal relation between the two.

In my next post, I wish to look at an experiment that allegedly falsified the hormonal hypothesis of obesity.  I believe I have some thoughts to contribute on the subject.

 

Does Cyrus Khambatta, PhD really “debunk” low carb keto diet claims? Part 3

This is the third of three posts where I examine a YouTube video by Dr. Cyrus Khambatta that debunks 7 low carb keto diet claims.  (see part1 and part 2).  I resume looking at the last three claims:

5.  Low fasting insulin means high insulin sensitivity.

Once again, Dr. Khambatta provides no sources.  He is absolutely right that a low fasting insulin does not necessarily mean that a person is insulin sensitive.  A proper test is indeed a glucose challenge, also known as Hyperinsulinemic-euglycemic clamp or glucose clamp technique.

But, once again, where are his sources?  Where does anyone claim that low fasting insulin alone proves that someone has a high insulin sesnsitivy?   Normally, ketogenic diet advocates make a more indirect claim, that a ketogenic diet will lead to weight loss which in turn is associated with increased insulin sensitivity.

What he is doing is mispresenting a perfectly valid method of estimating insulin resistance using what is known as the Homeostatic model assessment.  This method does use fasting insulin levels along with fasting blood glucose.

Talk about misleading statements!  He says, “Simply measuring your fasting insulin or fasting blood glucose independent of a glucose challenge is insufficient information to conclude anything about your insulin sensitivity!”

Well let’s fix that:  “simply measuring your fasting insulin or and fasting blood glucose independent of a glucose challenge is insufficient sufficient information to conclude anything about something your insulin sensitivity!”  The homeostatic model assessment will use both of these values to give a good estimate of your insulin sensitivity.

Note also, that there is good scientific research supporting the idea that very low carbohydrate diets will result in increased insulin sensitivity, for example, “Comparison of a very low-carbohydrate and low-fat diet on fasting lipids, LDL subclasses, insulin resistance, and postprandial lipemic responses in overweight women”, where it was found that a diet comprising less than 10% carbohydrate improved insulin sensitivity compared with others on a diet with less than 30% carbohydrate.

6.  “Low-carbohydrate diets are not high-protein diets”

Let’s ignore that this claim makes no sense at all.  If a person followed a zero carb diet consisting of mostly meat and high protein somehow does not qualify as low carbohydrate?  No one actually makes this ridiculous claim.

We know what he means.  A ketogenic diet may be defined broadly as a diet that causes you to get most of your energy from blood ketones.  You will find that there is not unanimity in the ketogenic diet community on this issue.  Regardless, the most common definition of a ketogenic diet is a high-fat diet, one where fat comprises 75 to 80% of the diet while carbohydrates are restricted to only 5% of the diet.  The other 15 to 20% is protein.  So, many, perhaps most of the ketogenic diet community are advocates of this high-fat version and warn of eating too much protein lest your body generates too much glucose from de novo gluconeogenesis and kick you out of ketosis.  Dr. Khambata is trying to dissuade these keto advocates from believing that their diet is not high in protein.  In the past diets high in both fat and protein are reported to cause health issues.  High fat keto advocates often emphasized the importance of not eating too much protein and describe their diet as moderate in protein, not high in protein.

Who is right?

Here Dr. Khambatta defines a high protein diet as anything more than 10 to 15 percent of calories.  Sure enough, high fat keto advocates are eating from 15 to 20 percent of their calories from protein.  But, the more common definition of high protein that you will find in the research is 25 to 30 percent of calories, not 10 or 15 or even 20.  For example, see this study where the high protein group consumed 30 percent of their calories as protein with the high protein group having much better lipid panel numbers.   That is contrary to his claim that the higher level of protein (at 15%?) leads to higher cardiovascular mortality.

Once again, I do not see Dr. Khambatta as an honest reporter of the facts.  In this case, he shows snippets from actual research, but without giving the references making it practically impossible to check if he has used the research correctly.  This is hardly the height of transparency.  It would be nice to actually see these reports and see what constitutes high protein in these cases, and what are the other nutrient components and what is the quality of the protein.  For example, studies performed using animal protein from casein must be regarded as suspect, since casein from “A1” milk is highly inflammatory (see https://www.larabriden.com/the-inflammation-from-a1-milk-is-mind-boggling).  As the saying goes, “the devil is in the details”, and Dr. Khambatta provides no details.

I will give him this:  He says, “it is practically impossible for a ketogenic diet to be low in protein.”   I don’t know about impossible, but he is right that it is difficult.  That is why ketogenic diet advocates emphasize monitoring your blood ketone levels with a meter or using urine tests.  I don’t see a real issue since most advocates are very clear on what is required to maintain that kind of very high-fat diet.

7.  Evidence-based research shows that low-carbohydrate diets are effective.

What?  He has a reference!  You have to capture the screenshot to be sure, but finally a reference.  Here it is:

 

I could only laugh when I looked this paper up.  Read it for yourself here.   Here is the conclusion of that study:

Conclusions: These initial results indicate that an individualized program delivered and supported remotely that incorporates nutritional ketosis can be highly effective in improving glycemic control and weight loss in adults with T2D while significantly decreasing medication use.

Now, it turns out that he does cite this as evidence of the benefits of a low carbohydrate study, but we are supposed to ignore this along with all of the other studies showing these benefits.  See for example this summary of 23 such studies, because none of them are long-term enough.  Once again, he gives no reference, absolutely nothing, to show that any long-term studies show that ketogenic diets have all the negative effects that he proceeds to list in a new laundry list of disastrous effects:

• Increased cardiovascular disease
• Hemorrhagic stroke
• Hypertension
• Atherosclerosis
• Diabetic mortality
• Obesity
• Cancer
• All-causee mortality

The truth is that all of this is bunk.  No such long-term studies of ketogenic diets exist.  This Dr. knows that such large-scale long-term studies are very expensive and have limited payoffs, so no one funds research at that level.  Short-term studies, however, show lots of benefits from this kind of diet including health benefits.  For example, see this review from the European Journal of Clinical Nutrition showing benefits for cardiovascular disease, type 2 diabetes, Epilepsy, acne, cancer, polycystic ovary syndrome, neurological diseases, Alzheimer’s, Parkinson’s, brain trauma, amyotrophic lateral sclerosis, and respiratory function.  (See, we can come up with laundry lists too! and provide evidence!)

There are findings, however, from long-term studies that do support the claim that ketogenic diets are helpful.  For an example, see my post on LDL cholesterol that describes benefits I experienced from bouts of ketogenic dieting and fasting. I draw on a presentation by Ivor Cummins who presented data from the Framingham Heart Study and The Münster Heart Study (PROCAM), both long-term, used to support facets of ketogenic diets.

But, I think we know what long-term study Dr. Khambatta has in mind.  It is The China Study which is supposed to prove the superiority of vegan diets over meat eating diets.  This study is hardly uncontroversial.  The primary promoter of this study and book is Dr. T. Colin Campbell.  It is known that he strongly advocated for veganism prior to his involvement in this study, so it is not inconceivable to suspect confirmation bias at work, and the China Study is not without its detractors (see also The Truth About the China Study).  but even if we accepted the China Study at face value, what is the China Study comparing?  Does it compare vegan diets versus ketogenic diets?  No.  At best it compares traditional starched based nearly vegan Chinese diets with modern diets introduced into China’s eastern cities wear not only higher meat consumption occurred, but also other ills of industrial civilization such as higher sugar consumption, refined vegetable cooking oils, and greater industrial pollution.  There are so many confounding factors and ketogenic diets, in particular, were never looked at.  If I am right, all I can say is that none of the scary claims made by Dr. Khambatta in his laundry list are justified by this data.  If I am wrong, then will the good Dr. please present his evidence?  Any evidence at all?  Because this video appears to have none.

 

 

Does Cyrus Khambatta, PhD really “debunk” low carb keto diet claims? Part 2

In my last post, I started examining a YouTube video by Dr. Cyrus Khambatta that debunks 7 low carb keto diet claims.  I covered three of these showing why I believe he debunks straw man arguments and displays poor and uncharitable reasoning. I covered the first three debunked claims. I cover the last three claims in my next post.  I resume now with the fourth claim:

4.  Carbohydrate is not an essential nutrient.

He calls the statement technically true!  So what’s the problem?  He claims that when keto advocates say this or something like it that they imply that “there is no use for glucose in the human body”.  Again, he offers no reference to anyone who says anything like that.

When keto advocates say something like that carbohydrate is not an essential nutrient, they reassure keto dieters that no nutritional deficit will arise from being in ketosis, not that glucose has no use in the human body.  Once again, this Ph.D. scholar fails to actually address anything keto advocates actually say but instead constructs something from his own imagination to knock down.  Once again, we are presented with a straw man argument, but one that isn’t even based on statements said by any advocate of ketogenic diets.

And, he misleads again…

“your brain can only run off of glucose for energy”.

He says this after eliminating Amino Acids or Fatty Acids as a possible fuel source for the brain showing them x’ed off in an illustration.  But we all know that the brain does very well using ketones (Beta–hydroxybutyrate (BHB) mostly plus acetoacetate and acetone) for up to 75% of its energy needs.  Ketones are manufactured in the liver from fatty acids.  That means the brain does use Fatty Acids indirectly for fuel.  Ketogenic diets, by the way, are not devoid of glucose, carbohydrate is included in the diet, albeit at levels low enough to enable ketosis.

He gives a laundry list of “Long-term Side Effects of Ketogenic Diets”:

diarrhea, nausea, constipation, vomiting, acid reflux, hair loss, kidney stones, muscle cramps or weakness, hypoglycemia, low platelet count, impaired cognition, inability to concentrate, impaired mood, disordered mineral metabolism, stunted growth in children, increased risk for bone fractures, osteopenia and osteoporosis, increased bruising, acute pancreatitis, hyperlipidemia, high cholesterol, insulin resistance, elevated cortisol, heart arrhythmia, myocardial infarction, menstrual irregularities, amenorrhea, and an increased risk of all-cause mortality. 

Wow, quite a list.  Is there any chance that he is misleading again?  Also, it would be really helpful if he could name at least one source to back up some of these claims.

Throwing out such a long list of unsubstantiated claims is a type of fallacy of its own.  It is a many questions or complicated question fallacy.  If we can shot down a few, the others might still stick, but let’s take a look:

Increased all-cause mortality. This likely comes from this study: Low-carbohydrate diets and all-cause mortality: a systematic review and meta-analysis of observational studies.  The study concludes that low carbohydrate diets are associated with an increased risk of all-cause mortality.  What’s the problem here?  The low carb diets under consideration where not ketogenic diets. CarolT, an admin at Ketogenic forums, has a comment reviewing the studies used for the “survey” (see https://www.ketogenicforums.com/t/help-with-scientific-studies/15536),  She derived the carbohydrate calorie percentages from a table that accompanies the article.  They are as follows:

Median intakes of carbohydrates, protein and fat in subjects with LCHP scores 2-20 ranged from 61.0% to 38.6%, 11.3% to 19.2% and 26.6% to 41.5% of total energy intake.

 

As Kristin Rogers comments on the ketogenic forum page, “This is not terribly low carb – 38-60% of calories from carbohydrate.”  And I will add that these clearly are not ketogenic diets.

 

Hyperlipidemia, high cholesterol, insulin resistance.  Really?  Check out this study of Long-term effects of a ketogenic diet in obese patients.  The conclusions state:

There was a significant decrease in the level of triglycerides, total cholesterol, LDL cholesterol and glucose, and a significant increase in the level of HDL cholesterol in the patients. The side effects of drugs commonly used for the reduction of body weight in such patients were not observed in patients who were on the ketogenic diet. Therefore, these results indicate that the administration of a ketogenic diet for a relatively long period of time is safe.

No glucose issues, no hyperlipidemia, cholesterol numbers outstanding.  What data is this “doctor” using?!

I think he picked up some of his laundry list of issues from this article: Ketogenic Diet Side Effects.  What you find from there is that many of these side effects are temporary or as the article says, “These effects tend to improve when the diet is continued, as the body adapts to the new diet and adjust the ways in which it sources energy.”

Some effects are real for some.  The aforementioned article said that 5% of patients suffered from kidney stones, but it adds that the condition is “treatable and the current recommendations suggest that the diet should be continued.”

A real significant known effect is on children.  “Children following the ketogenic diet may be affected by stunted growth, due to reduced levels of insulin-like growth factor 1.”

Now, adults need not be concerned with stunted growth and reduced IGF-1?  No.  In fact, lower IGF-1 levels are commonly touted as a benefit of vegan diets because it is believed to be carcinogenic.  What’s up with that?

I believe what I have already found discredits half of this list including the most critical claims.  Need I do more?  Maybe I will but at another time. This laundry list has taken a bit of time so I will resume with the last three points tomorrow.

But, I hope you can recognize that the credibility of this video is not very good.

 

Does Cyrus Khambatta, PhD really “debunk” low carb keto diet claims?

Cyrus Khambatta, Ph.D. of masteringdiabetes.org in a youtube video posted by plantbasednews.org “debunks” 7 misleading statements by low carb keto diet advocates.  You may view the video here:  LOW CARB KETO DIET – Debunking 7 Misleading Statements.

I found this from a posting in the “Ketogenic Intermittent Fasting” Facebook group.  I’ve joined a lot of Facebook groups lately, ones that have to do with diets and fasting.  I am investigating and experimenting with these to improve my own health.   I have not yet settled on a particular diet to follow long term, but I have found a ketogenic diet to be helpful with starting longer term fasts.  I viewed the video with some interest, and it has some good points to make, but I was seriously disappointed in the blatantly bad logic employed by someone claiming to be a Ph.D.  So, I thought I would reply to the points in this video.  It is relatively long.  So I have broken this up into three parts (part 1, part 2, and part 3).

Here are his first three “debunked” claims that keto advocates make and my response:

1.  Insulin is your fat storage hormone.

He does not deny that the insulin signals the shutdown of the release of fatty acids from fat and the increase of fat storage. In fact, he describes one of the functions of insulin is to “transport fatty acids to be burned for energy or to be stored as triglycerides” — also known as fat. That is fat storage! That is what you will learn from any textbook on dietary nutrition!

No keto advocate has said anything different. He implies with no references that ketogenic advocates claim something different that is false.

Perhaps he thinks they are claiming that insulin is primarily for fat storage, but no one has said that. And no one blanketly condemns the role of insulin in metabolism. These are false claims and a false characterization. He makes a classic strawman argument.

2. Eating carbohydrates spikes [sic] your blood glucose.

Another false claim! The normal keto claim is that eating high glycemic carbohydrates such as sugar and processed foods will spike blood glucose in most people. Does he deny that? No one claims that eating any carbohydrate will spike your blood sugar. He admits that when you eat carbohydrates that your blood sugar will rise. Also, no one claims that you should pay attention only to carbohydrate intake or that carbohydrate is the one single item that controls your entire blood glucose profile.

This is another obviously bad strawman argument.

And talk about misleading. He says, “Your blood glucose is primarily determined by how much fat you eat!” Is he saying eating fat spikes blood glucose levels? That is clearly false. But we can read between the lines to determine what he means.  Eating high-fat meals contribute to insulin resistance. No one denies that. However, the key point is that high fat does this only in the presence of high insulin levels triggered by an accompanying high carbohydrate load — think pizza, or ice cream or any one of hundreds of SAD food abominations all downed with a can of coke. Eating a ketogenic diet keeps insulin levels lower, permits the release of fatty acids from the tissues, and does not promote persistent insulinemia. By implying keto advocates say something different is very misleading and is another strawman argument.

He goes on to admit that a ketogenic diet keeps your blood sugar level low and stable, but then he makes another misleading statement. “but the minute you choose to eat carbohydrate-rich foods such a banana, a potato, or a bowl of quinoa your blood glucose is likely to increase significantly due to a hidden state of fatty-acid induced insulin resistance.”

Does he realize that this occurs when someone is in ketosis precisely because of the presence of FFA and ketones in the blood? And that it is very temporary? In the presence of carbohydrates, the body will drop out of ketosis. Once the fats and ketones are cleared from the blood the temporary state of insulin resistance will clear up rapidly. It is not due to any inherit insulinemia or incipient type 2 diabetes. And we agree completely about SAD! I don’t have any argument regarding whether a vegan diet that avoids sugar is effective in preventing insulinemia. Maybe it is, but what does that have to do with the effectiveness of a ketogenic diet?

3. Diabetes is a state of carbohydrate toxicity and insulin resistance is a state of carbohydrate intolerance.

Wow, it sure would be nice if he could give some sources. Is he saying that carbohydrates in sufficient quantities are not toxic to type 2 diabetics? Or that type 2 diabetics tolerate carbohydrate intake? Tell that to all those poor people who enter a diabetic coma from eating too much sugary food.

This is also a strawman argument. When a keto advocate describes diabetes in these terms, it does not mean that they are defining diabetes this way. We all know the definition of type 2 diabetes (insulin resistance resulting in abnormal metabolism and elevated blood glucose). He implies that keto advocates by using descriptions like this are giving out false definitions. Not so.

Also, is insulin resistance caused by high levels of insulin? Well, if you regularly inject non-diabetic people with insulin over a longer period, they will get fat and become insulin resistant. Doesn’t that justify a connection here?  I can agree that merely saying that insulin causes insulin resistance is an oversimplification, but there is a reasonable rationale to justify the idea that high insulin does, in fact, cause insulin resistance.

More to follow.

Is High LDL always bad?

 

In my previous post, I discussed my most recent blood lipid panel and discussed how much improved my triglycerides and HDL are compared to anything I have had in the last 30 years.

For review here were my most recent Lipid Panel numbers:

• Total Cholesterol     265  mg/dl    or    6.85 mmol/l
• HDL Cholesterol        62  mg/dl    or    1.60 mmol/l
• LDL Cholesterol       183 mg/dl     or   4.73 mmol/l
• Triglycerides              87  mg/dl    or    0.98 mmol/l

Triglycerides are supposed to be below 150.   They are 87.  HDL is supposed to be greater than 40.  It is 62.  More recent standards now focus not only on the absolute cholesterol levels but on the ratio of total cholesterol to HDL.  Here are the guidelines:

Total cholesterol-to-HDL ratio and heart disease risk:

• 3.4 signifies half the average risk for men (that would be 3.3 for women).
• 5 signifies average risk for heart disease for men. (4.4 for women).
• 9.6 signifies about double the average risk for men. (7 for women).

See Making sense of cholesterol tests.

My ratio is 4.3 which indicates a below average risk for heart disease even though I have high total cholesterol and LDL.

Now, as I mentioned in my last post, my test was taken three days into a water only fast and after eating a ketogenic diet for some days prior to the fast.  As explained then this would likely artificially boost my LDL numbers.  So, after over a week of normal eating, I took a home test of my cholesterol levels.   I read 225 for total cholesterol and 65 for HDL, making my LDL out to be 160.  But, I don’t trust my reading of the test so I won’t vouch for the accuracy of that reading.   I do think it confirms that my LDL lowered a good bit from my lab test, but that is all I think I can really say from that home test. But, if accurate, my ratio would be 3.4 signifying half the average risk for heart disease.  I require a new lipid panel to know for sure.

Here are some charts pulled from a talk by Ivor Cummins on the Primary Causes of Early Mortality.

The first one is based on the data I give above using data from the well known Farmington Heart Study:

Note the use of European measures in this graph.  In my case with an HDL of 1.60 and LDL of 4.73, I am right at the top of the very low range for any risk of heart disease.

But the cholesterol ratio is not the only factor to consider.  Triglyceride levels are also predictive.  The lower the triglycerides, the better.  Here is another graph from Ivor’s talk:

This data is from the The Münster Heart Study (PROCAM)

This graph uses the ratio of LDL to HDL instead of the total cholesterol to HDL.  In my case that would be 2.95.  Individual with a high ratio, but relatively low triglyceride levels below 200 had only half the number of Cardiovascular Heart Disease events as those with high triglycerides.  However, if your ratio is good and your triglycerides are low, then you risk is much smaller.

I did show very high LDL levels in my recent lab test.  From my home test it would seem that they are still high, if not as high as during my fast.  Regardless, it does seem that my heart disease risk is now much lower than it has been in many years due to the much improved HDL and triglyceride levels.

One last graph before I go.  It is well known that not all LDL cholesterol is alike. LDL is used to transport fat around the body, particularly from the liver to cells for use or storage.  LDLs that are “full” are large and buoyant.  These large and fluffy LDL particles cannot penetrate arterial cell walls to form plaques.  As such, they are not “bad” at all.  The truly bad cholesterol are LDLs that have released their stores and turn into small dense LDLs that are the ideal size to penetrate small arterial injuries or cuts and embed themselves causing an immune response and the formation of arterial plaque that calcify and harden your arteries.

There is a relationship between triglyceride levels and LDL particle size.  In general, the lower your triglycerides, the greater the percentage of LDL is of the large buoyant kind.  And that is good.  Given my rather low triglycerides, I have reason to believe that my heart disease risk is even lower than indicated by my cholesterol ratio alone.

This graph a prettier version of one in the original article (Atherogenic Lipoprotein Phenotype A Proposed Genetic Marker for Coronary Heart Disease Risk).

Fasting for Health!

Fasting.  Going without food or drink for an extended period of time.

There are all kinds of fasts, but the fasts I looked at and practiced were no calorie fasts or water only fasts.  In no case did I consider any kind of fast that required not drinking water!   I don’t see a lot of research on dry fasting, but I do see many warnings of its dangers, but that is a topic for another time.  The fast that I considered and practiced were no calorie fasts, some of which were water only fasts.  Liquids are permitted on these no calorie fasts, mostly water, but other liquids such as tea or coffee or bone broth would be permitted.

Since last November I’ve fasted about 15 days with 5 days being the longest in length.  In all but my most recent fast, I made the mistake of not drinking enough water.  I intended the fast that lasted 5 days to go longer, but my legs started to hurt very badly.  After I drank some water, the pain subsided only to return an hour later.  Since I had a long auto trip and responsibilities the next day, I elected to end the fast at that point.  It is better to proceed cautiously in these matters.

Drinking water on these fasts is particularly important in order not to get dehydrated.  A good guide is to drink (in ounces) about half your body weight (in pounds).  I just completed a 3 day fast, but I made sure to drink lots of water.

In preparation for each of these fasts, I ate a low carbohydrate high fat or LCHF diet for a few days.  My diet for the last several months has been mostly LCHF, but not ketogenic.  What is the difference?  Well, there are many LCHF diets.  Any diet where the amount of dietary fat is greater than 50% of the calories you eat in a day while keeping protein constant can be called LCHF.  All such diets will, given some time, reduce the average level of insulin in the blood in people who suffer to some degree with hyperinsulinemia or high blood insulin levels.  A ketogenic diet is a more restrictive form of LCHF diet.  It requires that 75% of your daily calorie intake consist of fat, and only 5% consist of carbohydrate with the remaining being protein.  The very low carb and moderate protein causes your body to burn up its stores of glucose and to convert to burning fat.  When glucose (blood sugar) is not available, your liver will convert fatty acids to ketones** which most of your body can use directly for energy in place of glucose.  This is a state of nutritional ketosis.***

To be clear, in the days before I started any 3 or 5 day fast, I ate a strictly ketogenic diet for a few days in order to induce nutritional ketosis before I began the fast.  I believe this helped the fasts to be more effective, but my reason was psychological. I simply found it easier to resist eating at the start of a fast after being in nutritional ketosis.****   I was able to cook and prepare food for others and be around food without succumbing to foods allures.

How did this affect my health?   On this I don’t have concrete before numbers to share, so all I can give is my testimony.  In all three previous blood tests I had in the last 20 years, my cholesterol was high, my triglycerides were high and in the two more recent tests prior to this year, my HDL was low.  But since last August, I have sharply reduced my sugar consumption, and in the last three months have fasted for 15 days in total.

I have now had a new set of blood tests.   I made a mistake, however, in having these test done on the third day of a fast, a fast that followed most of a week of nutritional ketosis.  That’s important.

Here were my most recent Lipid Panel numbers:

• Total Cholesterol     265  mg/dl    or    6.85 mmol/l
• HDL Cholesterol        62  mg/dl    or    1.60 mmol/l
• LDL Cholesterol       183 mg/dl     or   4.73 mmol/l
• Triglycerides              87  mg/dl    or    0.98 mmol/l

(See http://www.onlineconversion.com/cholesterol.htm for a conversion tool to convert between American and European units of measure.)

The problem with these measurements is that my 3 days of fasting and prior ketogenic eating has likely distorted the numbers from what they would be on a more normal diet.   The high LDL Cholesterol is of major concern to my doctor.

Nevertheless, I found great encouragement in the relatively high HDL and low Triglycerides.  The medical profession looks for HDL values to be greater than 40 and for triglycerides to be under 150.   These are huge improvements over anything I have had for the last 30 years.

The high LDL is likely due to the fasting.  I was tipped off to this phenomena by the self-experimentations performed by David Feldman, a software engineer by trade, but someone who has made a name for himself in the world of Ketogenic diets.  Normally, people on ketogenic diets report excellent improvements in lipid blood panel numbers.  But David is an exception.  He is what is called a hyper responder.  While on a ketogenic diet, his blood cholesterol skyrocketed and remains high.   That lead him to undertake a series of experiments accompanied by an epic level of blood testing.  What he found is worth reading about at www.cholesterolcode.com.  One of his experiments was with a 3 day fast to see what effect, if any, a fast had on cholesterol levels.  Sure enough, after the fast, his LDL cholesterol (aka LDL-C) shot up 84 points.  It returned to pre-fast levels after refeeding.  His HDL cholesterol was unaffected.  You can read about it here: cholesterolcode.com/the-fasting-disaster/

The spike in LDL is easily explained. LDL carries fat in the blood to the tissues for burning. When you are fasting, you necessarily draw on your fat stores for energy and will require more LDL for transport.

There is good research backing up my belief that fasting temporarily elevated my LDL. See Fasting Increases Serum Total Cholesterol, LDL Cholesterol and Apolipoprotein B in Healthy, Nonobese Humans.  Ten non-obese healthy adults fasted for seven days.  During that time:

• The average total cholesterol went from 4.90 to 6.73 (189 to260).
• The average LDL cholesterol went from 2.95 to 4.90 (114 to 189).
• HDL and triglycerides were unaffected.

So, my double efforts having greatly reduced by sugar consumption and fasting appeared along with some LCHF eating appears to have paid off in two ways.  My HDL and my triglycerides are much improved and are pretty good.

 

 

 

 

 

** The common ketones are beta-hydroxybutyrate (BHB), acetoacetate and acetone.

*** Being in nutritional ketosis is not the same as being keto-adapted.  Once you are in nutritional ketosis, the body will make changes and adaptions of many types that will take a few weeks (up to 12 weeks in some cases) before you are keto-adapted. Also, nutritional ketosis should not be confused with ketoacidosis, a serious medical condition that occurs in type 1 diabetics when they do not get their insulin.   The body will have both high blood sugar as well as high blood ketones which the liver produces due to very low insulin levels.

**** There is a simple explanation for this also.  When your stomach is empty, it secrets the hunger hormone ghrelin causing you to feel hunger.  After you eat, the level of ghrelin drops within the next hour or so.  But, if you ate primarily carbohydrate, the ghrelin levels will subsequently go back up.  But if you ate primarily higher protein or fat, the ghrelin levels stay down for much longer.  We commonly experience these phenomena when eating Chinese food, known for being high in carbohydrates.  Once we eat it, we are hungry again not long after the meal, but more fat laden meals satiate us for much longer.

Giving up Sugar.

What can older people like myself do to improve their health and increase their chances of living longer?   I am exploring these and looking to improve my own situation and outlook.  So, in my initial post I talked about my body mass index (at 28.6 I’m overweight), my blood pressure was high, and I had metabolic syndrome.  The key word there being had.

Last summer, I determined to bring about changes in my life and dietary habits.  I did only one thing consistently.  I gave up consuming sugar.  I did not drink soda often anyway, but I gave it up entirely and gave up my favorite sweet iced tea.   And I gave up sweets of any kind, donuts, and most processed foods.  My inspiration for all of that was Dr. Robert Lustig’s famous video, Sugar, The Bitter Truth.

Sugar makes you fat!

The link between sugar and obesity is evident looking at statistics from the late 20th century.  The percentage of the population that was obese essentially doubled in all categories since 1980.  For example for people aged 45 to 64, the percentage of the population that is obese increased from 20% to about 40%.  As sugar consumption rose, so did obesity.

However, starting in 1999, the per capita sugar consumption in the US started to go down, while obesity rates continued to climb.  A respected neuroscientist, Dr. Stephan J. Guyenet, used this data to suggest that sugar consumption is not a unique cause of obesity.  He produced the following graph as evidence:

This looks pretty convincing does it not?

Well, it shouldn’t.  Gary Taubes (author of The Case Against Sugar), criticizes this evidence and Dr. Guyenet’s conclusions pretty decisively in an article, The Case against Sugar Isn’t So Easily Dismissed.  He points out that the sugar consumption levels remain very high and that the per capita decline in the consumption of sugar in the 21st century is very modest.  The graph deceptively exaggerates the drop.  I redrew the graph as follows:

But the fact remains that sugar consumption is going down.  Does this suggest that sugar is not the most significant cause of America’s obesity epidemic?  Not really.  The assumption behind that conclusion is that these trend lines will always correlate one to one.  But they won’t because the obesity percentage represents a cumulative effect of past behaviors, while the per capita sugar intake is not cumulative.

For example, if I ate 110 grams of sugar a day and got fat as a result, but if I then reduce my sugar intake to 93 grams a day, will I then become thin?  No.  A modest reduction in sugar consumption will not reverse the damage, and if I continue to eat sugar at that lower rate I will continue to get fat, just maybe at a slightly slower rate.  Similarly, the number of new cases of obesity will continue to rise because the sugar consumption remains high, but the rate of growth will slow. And that is exactly what we see in this graph. When the decline began, the climb in the percentage of obesity slowed.  The graph, in fact, makes the correlation a bit stronger, not weaker.

I personally have no doubt that sugar consumption is a health care disaster. But we should remember that correlation does not always equal causation.  For example, fat people wear bigger clothes.  That’s a strong correlation, but it does not show that big clothes make people fat.  For sugar, however, we now have enough scientific research to show the causal connections.  One such paper is Fructose and NAFLD: The Multifaceted Aspects of Fructose Metabolism.  This paper shows that excess sugar consumption can lead to liver damage, inflammation and “leaky gut” issues,  but insulin resistance leading to type 2 diabetes is the primary risk.

What does insulin do?  Insulin is a hormone secreted by your pancreas.  Insulin’s job is to tell the body to store energy.  It is the energy storage hormone.  So, insulin signals your cells to open up and accept both fat (triglycerides) and blood sugar (glucose) to use or store.  Additionally, it prevents the cells from using stored glucose and fat for energy.

What causes insulin resistance?  Again we have good research indicating that it is “Visceral adiposity” or fat found in the muscles, liver and around the vital organs in your body.  It’s fat inside our muscle cells and liver.  I give links to research papers below that show this link.  The mechanism is no mystery.  If your fat cells get filled up with excess energy in the form of fat or glucose, some of which gets converted to fat, then it may simply get too full and resists receiving any more.  It ignores the signal that insulin gives.  But, sustained high blood sugar levels are dangerous to the body, so the body puts more insulin into the blood causing a condition known as Hyperinsulinemia.  The increased signaling does cause the cells to store more fat and glucose, but over time, there is a diminishing return.  When the process breaks down over a period of years, you get Type II diabetes.

But how does sugar cause fat in cells?

I’ll try to explain.  Sugar or sucrose consists of sucrose molecules.  The sucrose molecule is the union of a glucose molecule and a fructose molecule.  The glucose molecule is relatively benign.  It is simply, the main fuel source for the body.  However, when you eat sugar,  your blood glucose levels tend to rise rapidly resulting in a rapid rise in blood insulin levels.

Fructose, however, does not enter the bloodstream.  Rather it is processed by the liver.**  There some of it gets converted into glucose and lactate (simple sugars the body uses as fuel) and the remaining gets converted into triglycerides or fat.  If fructose levels are too high, the mechanisms that convert fructose to glucose are overwhelmed and most of the fructose gets converted to fat.  This process goes by the name hepatic de novo lipogenesis which are Latin words describing new fat generation by the liver.

This fat is stored in the liver or released into the bloodstream as triglycerides.   By the time this happens, a person’s insulin is elevated due to the increased blood glucose from the other half of the sugar molecule.  The elevated insulin turns on the bodies energy storage mechanisms telling the body to store fat in the liver and adipose (meaning fat) tissue.  The fat that gets stored consists of triglycerides created by the liver from fructose.  Eating lots of sugar over time causes the build-up of these Intramyocellular lipids or the fat inside our muscle cells that create insulin resistance.

Fructose makes you overeat!   

From the article Sugar consumption, metabolic disease and obesity:  “Mechanistically, it is plausible that fructose consumption causes increased energy intake and reduced energy expenditure due to its failure to stimulate leptin production.”  Normally, when you eat, your body decreases levels of the hunger hormone, Ghrelin, and increases Leptin, a hormone that inhibits hunger.  Fructose by-passes normal digestion by being processed in the liver.  As such, it fails to stimulate leptin, so you continue to eat more than you would when eating other foods.

Fructose in large doses can cause other serious issues.  A rapid rise in liver fat causes inflammation in the liver or fatty liver disease.  Fructose not absorbed by the liver, that passes into the large intestine where the wrong gut bacteria feed on it, causes changes that reduce the gut permeability.  There is a mucus that lines the inside of your intestines that protects you from compounds in your food that can cause you harm.  When this mucus is reduced, your gut is more permeable and can let in some of these compounds into your bloodstream.  This is what is meant by having “leaky gut” or “leaky gut syndrome”.

So, my first step in recovering my health was to eliminate sugar as much as possible.  That means no adding sugar to any food I make, avoiding any sweetened beverages, avoiding sweets of any kind such as ice cream, pastries, and cakes, and avoiding almost all processed food, 80% of which has added sugar.

Next:  Fasting. How removing sugar and fasting improved my health.

** See an article below.  There is evidence that some fructose may be converted to glucose in the small intestine, but the operative word there is small.  It is consistent with the idea that we are created to process small amounts of fructose that we get from fruit, but larger amounts are essentially a toxin similar to alcohol.

Here are a few research papers showing the link between fat and insulin resistance (there are many others):

Intramyocellular lipid concentrations are correlated with insulin sensitivity in humans: a 1H NMR spectroscopy study.

Visceral Adiposity, Insulin Resistance, and Type 2 Diabetes

What causes the insulin resistance underlying obesity?

A figure from that last article:

And here are some research papers showing the link between fructose and the increase in visceral adipose tissue or fat:

Sugar consumption, metabolic disease, and obesity: The state of the controversy.

Metabolic effects of fructose and the worldwide increase in obesity.

Fructose metabolism and metabolic disease.

Here is a more recent research paper that absolves fructose so long as the amount consumed remains small, such as the amount you might get from a piece of fruit: The Small Intestine Converts Dietary Fructose into Glucose and Organic Acids.  I think it’s worth quoting:

“Low doses of fructose are ∼90% cleared by the intestine, with only trace fructose but extensive fructose-derived glucose, lactate, and glycerate found in the portal blood. High doses of fructose (≥1 g/kg) overwhelm intestinal fructose absorption and clearance, resulting in fructose reaching both the liver and colonic microbiota. Intestinal fructose clearance is augmented both by prior exposure to fructose and by feeding. We propose that the small intestine shields the liver from otherwise toxic fructose exposure.”

What this tells us is that fructose in the low doses you find in whole foods are harmless, but large does are toxic when reaching the liver and the colonic microbiota.

 

 

Images from https://www.ncbi.nlm.nih.gov/books/NBK19623/figure/chartbook.f7 showing the doubling of obesity in the USA since the 1970s.

The latest government averages:

From from Stephan J Guyenet, The science of body weight and health.  Based on The latest CDC data on obesity.