Human Digestion & Metabolism for Fat Heads
Tom Naughton has weighed in with some random musings regarding ketosis: Reactions To Arguments About Ketosis. The more Fat Head talks about nutrition the more evident it becomes that he really has no idea what he is talking about, and really ought not to be educating anyone no matter how entertaining he thinks he is.
Ketogenic diets are stupid because everyone apart from diabetics should be able to consume at least 150 grams of carbohydrate per day.
I don’t think the everyone should eat starch argument makes any more sense than the no one should eat starch argument. All humans have the AMY1 gene, which makes it possible to digest starch. That’s one of the many reasons I believe our paleo ancestors ate starchy plants. But some clearly ate a lot more than others. Let’s review a quote from Denise Minger’s book Death By Food Pyramid:
It turns out the number of AMY1 copies contained in our genes is not the same for everyone. And the amount of salivary amylase we produce is tightly correlated to the number of AMY1 copies we inherited. AMY1 copy number can range from one to fifteen, and amylase levels in saliva can range from barely detectable to 50 percent of the saliva’s total production. That’s a lot of variation.
It sure is. And that means some people can handle a whole lot more starch than others. Research shows that people with fewer copies of the AMY1 gene are more likely to be obese. To quote a study I mentioned in a previous post:
The chance of being obese for people with less than four copies of the AMY1 gene was approximately eight times higher than in those with more than nine copies of this gene. The researchers estimated that with every additional copy of the salivary amylase gene there was approximately a 20 per cent decrease in the odds of becoming obese.
The AMY1 gene thing had been in the news back in April, and I blogged on this at that time. I'm always fascinated by the seeming desire in this community to find a singular factor in all of this and jump at any seemingly supportive observation without what appears to be much thought. The NoraG keto crowd in the IHC believes that we evolved to eat very low carb high fat diets, and her credo is the fewer carbs in life the better. The problem is that the human genome in the context of evolution poses some problems for this. Why would amylase have persisted if we didn't consume starches? This was the major thing I took away from Chris Masterjohn's discussion of AMY1 at AHS12. Not only do we see the gene, but the number of copies is greater in cultures that are known to have consumed higher starch diets.
Then in April, this paper was published in Nature: Low copy number of the salivary amylase gene predisposes to obesity. I discussed the obesity angle back then and won't really repeat it now, but I want to make a few points. The studies looked at the association between gene copy number and obesity. How many times does Tom or Denise or myself or anyone have to repeat that correlation does not equal causation? And yet, that word in the title of the paper -- predisposes -- at least implies causation. Tom's statement, "with every additional copy of the salivary amylase gene there was approximately a 20 per cent decrease in the odds of becoming obese", implies causality. When we talk "risk factors" there is the implication of cause and effect. Isn't this what we are supposed to be smarter about vis a vis cholesterol?
The thing about cholesterol is that we do have a pretty good handle on mechanisms that can reasonably explain how elevated LDL causes atherosclerosis. Now while these plausible mechanisms may some day be discredited -- as reasonable scientific hypotheses through the ages have been -- they are nonetheless miles ahead of hypotheses that are nothing more than wild conjecture, often not even educated.
The AMY1 gene story in the IHC is a perfect example of bad science. This is what happens when you take a B- physics student turned journalist's hypothesis, accept his insistence that it be the null hypothesis, and jump at every observation and view it through the lens of how it could support that hypothesis. This is not how science is supposed to work. Hypotheses are supposed to be formulated to explain observations. Then, hopefully, these can be tested through experimentation. Gary Taubes' hypotheses (there are multiple ones combined to form his gran mal hypothesis that carbs make us fat) were not formulated from observation or we wouldn't be in this situation where so many "educated" folks believe that carbohydrates cause insulin resistance and diabetes. His more nuanced versions of the hypothesis focus on IR being a prerequisite or cause of obesity and not the other way around.
This model of obesity (and diabetes) was tearfully put forth by Taubes side-kick Peter Attia at a TED-Med talk, and is also the main thrust of Fat Head's aptly named DVD, Big Fat Fiasco. In BFF, Tom rolled out this notion that you are only as fat as you need to be to maintain blood glucose levels. Once your muscles are IR, carbs are taken up by the fat cells and converted to fat that is further trapped there by the insulin. You get fatter and fatter until the fat can't even take it anymore and you explode. Just kidding, you become diabetic. Yeah, that's how it goes in the world according to Fat Head. It is "carbohydrate intolerance" that causes obesity in their eyes. Furthermore, this carbohydrate intolerance is presumed to be inherent -- e.g. genetically determined -- therefore if the unlucky ones don't want to get fat, they must avoid carbs.
Thus Naughton interprets this AMY1 information in the context of his preconceived (yet unsubstantiated by the evidence) ideas on the cause of obesity. Low AMY1 are indicative of low amylase levels, and those with low amylase "can't handle" a whole lot of starch. If they eat starch they are therefore more predisposed to becoming obese as a result.
But this mechanism makes no sense and hopefully we won't be seeing Nashville Farms weight loss clinics any time soon.
What am I talking about? Well, I bring this up from time to time because it is instructive. Anyone remember the Beverly Hills Diet? I had a friend do this diet one summer and by the time she was three days in, I was gagging at the sight of a papaya! Judy Mazel did quiet well with the book and her weight loss clinic despite the fact that she had zero background and the diet had no scientific basis. The idea was that eating certain fruits that contained fat "burning" enzymes would burn fat. Only problem is that digestive lipases break down triglycerides so that they can be absorbed into the body, and have nothing to do with the lipases inside our bodies that serve the same function (and are still not involved in "burning" fat per se). Indeed, if BHD dieters had consumed any fat along with all that fruit, there's an outside chance they would weigh more due to better digestion.
Tom Naughton is making a Judy Mazel mistake, which is not surprising given that he, too, has no background in nutrition.
Starch is essentially a polymer of glucose, composed of many glucose molecules strung together. Digestive enzymes called amylases break down starch into glucose that can then be absorbed and utilized by the body. Note the use of the plural there, because there are two amylases in the human body: salivary and pancreatic. From my new favorite biochemistry text, Marks' Basic Medical Biochemistry p. 496:
Amylases have zero, zilch, nada to do with carbohydrates once in your body. If you are deficient in amylase, you would absorb less ingested carbohydrate. From a blood glucose point of view, you would be more "tolerant" of dietary carbohydrate compared with your amylase-rich friends. BUT:
In other words, amylase deficiency is rare. Further, this whole gene copy thing is for salivary amylase which neglects the contribution of pancreatic amylase.
If health and nutrition are not a concern, then what you want is poor digestion so that you can maximize consumption and maximize how much comes out the other end as closely resembling what went in as possible. I don't recommend this, but if weight loss at all costs is what you're looking for, there are a number of foods that can help you towards that goal. There are also a number of diet aids that work on this premise. Xenical now OTC as Alli, is a fat blocker. It is likely almost as effective for weight loss in preventing fat overconsumption from fear of soiling oneself as it is for the actual fat calories it blocks the absorption of. Starch blockers have been around in the OTC diet pill industry for as long as I can remember, and have even been employed in the treatment and management of diabetes. While older amylase inhibitors were not very effective for a variety of reasons, digestion-resistant ones have been developed that are to some extend. A quick search on amylase inhibitors turned up this study: A proprietary alpha-amylase inhibitor from white bean (Phaseolus vulgaris): A review of clinical studies on weight loss and glycemic control
... As an alternative to a low glycemic index diet, there is a growing body of research into products that slow the absorption of carbohydrates through the inhibition of enzymes responsible for their digestion. These products include alpha-amylase and glucosidase inhibitors. The common white bean (Phaseolus vulgaris) produces an alpha-amylase inhibitor, which has been characterized and tested in numerous clinical studies. A specific and proprietary product named Phase 2® Carb Controller (Pharmachem Laboratories, Kearny, NJ) has demonstrated the ability to cause weight loss with doses of 500 to 3000 mg per day, in either a single dose or in divided doses. Clinical studies also show that Phase 2 has the ability to reduce the post-prandial spike in blood glucose levels. ...
Speaking of glucosidase inhibitors, surely someone who has palled around with so many experts on low carb cruises has heard of Acarbose? Acarbose, like Alli, likely works at least in part by inhibiting carb consumption so as to avoid odorous side effects.
So the lesson for today is this: If you have a low amylase gene copy number, you are somewhat less likely to digest starch completely as your high copy number neighbor. If anything this would lead to lower glucose spikes following a carbohydrate rich meal and a greater tolerance of carbohydrates.
Furthermore, humans who have consumed high carbohydrate diets through centuries express higher numbers of AMY1 genes and produce more salivary amylase. The result of this, if any, would be enhanced digestion and uptake of glucose. This seriously undermines the notion that glucose is toxic if evolution based tenets hold. By that I mean, if glucose were toxic, the humans with lower assimilation would prevail over those with high assimilation. Dang that AMY1 doesn't seem like such a good argument for Fat Head Fables after all.
Tom wraps this part of the discussion up by telling his audience of his slide towards diabetes.
Why?I haven’t had a genetic test to determine how many AMY1 copies are floating around in my DNA, but given the difference in my weight and health on high-starch vs. low-starch diets, I suspect I’m in that under-four-copies group.
Okay ... but ...I usually eat two meals per day. To get 150 grams of carbohydrate into my diet, I’d have to consume 75 per meal. Not a chance. After supplementing with resistant starch, I’ve found I can have that potato or squash with dinner and end up with a post-meal glucose peak in the 125-135 range. I’m fine with that. So now I have a potato with dinner a few times per week.
But when I consumed two potatoes (i.e., about 70 grams of starch) awhile back as an experiment, my glucose ended up at 195 and stayed high for two hours. I’m not fine with that. And no, I don’t think it’s because I need to eat more starch to raise my tolerance.
Naughton has an impaired glucose stimulated insulin secretion response or GSIS. I'm willing to bet this wasn't the case back when he was filming Fat Head. It's not so much the spike (although over 200 at any given time = diabetes) but the sustained hyperglycemia (which is due to lack of insulin and/or lack of glucagon suppression so that endogenous glucose production proceeds unchecked) that is of concern. What it's not due to is lack of salivary amylase to "handle" the glucose.