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Sunday, February 3, 2013

Response to Dr. Paul Jaminet’s Rebuttal on Fructose



This rebuttal of sorts by Dr. Paul Jaminet was recently brought to my attention through a comment left on my Facebook page.  Danny Roddy was nice enough to lay out the arguments for me point by point.  Dr. Jaminet’s comments are in red.


1) “I think there’s substantial evidence that high fructose intake promotes endotoxemia” –PJ

This is not what I have found.

Diabetics and the obese have higher lipopolysaccharide (LPS) levels in their blood and they consume more fructose, primarily via HFCS, than people who are not diabetic or obese.   But as to specific food effects, the generation of LPS is buffered against on the ingestion of simple sugars because, for the most part, simple sugars are completely digested and absorbed in the upper part of the small intestines where microbial activity is minimal to non-existent. 

It is, however, conceivable that HFCS could lead to the generation of LPS because of the the presence of large starch molecules, if you recall.  Starch molecules, particularly when insufficiently cooked, can circumvent digestion and provide fodder for bacteria in the lower intestines, leading to the generation of LPS.

Endotoxemia occurs, though the definition is arbitrary, when blood levels of LPS rise by about 2- to 3-fold above normal levels.  Fats, in this regard, by permitting the passage of LPS into the body at high rates via newly made chylomicrons, execute the damages of LPS initiated by the increased proliferation of microbes in the intestines that was promoted by starches.


2) “The fact that many researchers use very high doses of fructose (in order to generate clear results in a reasonably short period of time) doesn’t prove that fructose is benign at lower doses” –PJ

This is a straw man.  I’m not saying that fructose is safe or beneficial merely because researchers employ high doses of it for the purpose of hastening the development of toxic effects in animals.  I’m instead saying that arguments should be established on studies in which fructose is (1) administered in the way it’s eaten in the real world (i.e., with glucose) and (2) given in more moderate and realistic doses (i.e., as reflected by consumption data).


3) “Kim seems to think it’s a good sign that “fructose ingestion induces thermogenesis”. However, in my view thermogenesis is a bad sign. It implies the presence of an energy excess (or a toxic macronutrient) which had to be disposed of.” –PJ

Diet-induced thermogenesis consists of (1) the energy costs of digesting, absorbing, and storing ingested nutrients and (2) the dissipation as heat, by the activation of the brown adipose tissue, which is blunted in obesity,1 diabetes,2 and old age, of ingested nutrients.

I don’t see this as a ‘bad sign’ or even the presence of ‘nutrient excess.’  This is because when isocaloric amounts of fructose and glucose are compared, studies show that fructose increases energy expenditure and total carbohydrate oxidation significantly more than glucose does throughout the whole body.  Studies also show that when fructose is exchanged calorie-for-calorie for glucose, weight loss becomes accelerated.

One way that fructose leads to greater thermogenesis than glucose is by shifting the cell’s energy charge.  Although this effect is subtle, fructose accomplishes this by (1) rapidly consuming phosphate via bypassing a key regulatory step in glycolysis and (2) by converting more readily to glycogen, while consuming twice as much ATP in the process, compared glucose.

Also, fructose, without insulin, apparently activates brown adipose tissue (that are loaded with uncoupling proteins) in conjunction with thyroid hormone, adrenalin, and noradrenalin3–5.  Nutrients, therefore, are processed for heat rather than energy (ATP).

To what extent diet-induced thermogenesis contributes to long-term body fat regulation, I’m not sure.  But fructose (and sucrose) is less likely to lead to an increase in body fat than glucose (and starch) because compared to glucose, the ingestion of fructose, as a conservative estimate, leads to a 10-fold greater increase in energy expenditure than glucose does for hours after consuming it.

Consider what would happen if you conducted a study, where 100 subjects were enrolled and instructed to consume a 2,000 calories diet, 50 percent of which would come from carbohydrates.  You then assign half of the subjects to consume only sucrose, and the other half of the subjects to consume only glucose for a year.

The subjects would eat 3 square meals a day, so they can be conceived to be in the “fed-state” for about 16 hours of the day. Again, we would employ the conservative estimate that fructose leads to a 10-fold greater increase in energy expenditure during the “fed-state” than glucose does.

So, let’s say that fructose increases energy expenditure by 0.08 calories per hour per gram of fructose ingested, and glucose increases energy expenditure by 0.008 calories per hour per gram of glucose ingested.  Based on these rates, fructose leads to an increase in energy expenditure of 320 calories over the course of a day.

(.08 calories/hour) x (16 hours) x (250 grams of fructose) = 320 calories.

Glucose, on the other hand, leads to an increase in energy expenditure of 32 calories over the course of a day.

(.008 calories/hour) x (16 hours) x (250 grams of glucose) = 32 calories.

Therefore, the sucrose only group would be expending an extra 176 calories per day (160 + 16), whereas the glucose only group would be expending an extra 32 calories per day.  At the end of the study, the sucrose only group would expend an extra 63,360 calories (175 x 30 x 12), whereas the glucose only group would expend an extra 11,520 calories (32 x 30 x 12)—a difference of 51,840 calories. 

Because a pound of fat contains approximately 3,5000 calories, simply replacing sucrose for glucose in the diet, changing nothing else, would, in theory, lead to a decrease of slightly less than 15 pounds of body fat over the course of a year (51,840 ÷ 3,500).


4) “…the healthiest diet is the diet that eliminates hunger with the smallest calorie intake.” –PJ

Rather than the one that terminates hunger, I posit that the healthiest diet is the diet that allows us to eat the most, while minimizing the likelihood of gaining weight.  In other words, the healthiest diet is the diet that keeps the body temperature and metabolic rate optimized.  After all, heat is necessary for optimal biochemical activity of enzymes throughout the body, and the continuous supply of energy (ATP) is the basis for the organization and functioning of living cells.  Carbohydrates serve these purposes well, and they do so much better than fats do.


5) “…We even know the mechanism by which this happens: fructose depletes ATP in the liver, causing the release of adenosine, which is degraded to uric acid.” – PJ on fructose and uric acid

This has been overturned recently.  It turns out that at least 200 grams of pure fructose is needed for the toxic, uric acid increasing effect to kick in.6

Fructose does, in fact, deplete ATP more than glucose does simply because of the nature of its metabolism, but the effect is subtle and not necessarily undesirable.  By rapidly depleting the high-energy phosphate bonds of ATP, fructose (1) forces glucose to be used at a higher rate and (2) depletes the reducing cofactor called NADH, which is a good thing (and a topic for a whole other post).

So, through these dynamic processes the excessive accumulation of ADP, AMP, and adenosine (which irreversibly diffuses out of the cell and is ultimately degraded to uric acid) is effectively kept in check, and ATP levels inside cells don’t decrease too much.


6) “I won’t go further through his whole series, I’ll just observe that it’s easy to go astray when you focus on molecular biomarkers, hormones, or short-term responses to meals…If you look at our book, very rarely do we mention any of the body’s hormones or intermediate signaling molecules and base any argument on their levels. We argue from evolutionary lines of argument, or from direct links between nutrients themselves and diseases. This greatly reduces the chances of going astray.” - PJ

I tend to stay clear of  ‘evolutionary lines of argument’ because they are subject to a bit too much speculation for my taste, put too much focus on “traditional diets” that differ wildly between populations, and ignore the experiments in which animals reared in “artificial” settings live significantly longer than their counterparts living in the wild. 

Diseases with direct links to nutrient deficiencies have been established, and for the most part, conquered in developed parts of the world.  Keshan disease, for instance, which is a syndrome that occurs where selenium is deficient in the soil, has been largely eradicated by the fortification of foods with selenium.  In parts of China where selenium is lacking, selenium is given in salt, and this practice has dramatically reduced the incidence of Keshan disease.

The subtleties of the effects of nutrients in the body, however, can only be appreciated with an integrated understanding of nutrients’ metabolism in the body, and this includes their interactions with hormones and intermediate signaling molecules.  Take for example iodine, which is needed for thyroid hormone synthesis.  Too much iodine suppresses the thyroid gland but when given in just the right amount, optimizes thyroid hormone synthesis.  Thyroid hormone, in turn, donates iodine to immune system cells called neutrophils that then, using iodine, produce bactericidal compounds to clear away infections.

This bidirectional effect of iodine on the thyroid gland occurs fairly quickly, so the anti-infective effect of iodine can’t be comprehended, nor can doses of iodine be properly titrated, in the absence of hormonal data.

Although I agree with Dr. Jaminet that the short-term effects of meals should be taken with a grain of salt, I don’t think that they should be all together ignored, as they can serve as cues for consequences to come.

For instance, people who have a tendency to become hypoglycemic several hours after eating are at a very high risk for developing diabetes.  This is because, in response to hypoglycemia, the counterregulatory hormones are released, and the habitual, intensive release of these counterregulatory hormones over time could lead to insulin resistance and inhibit insulin secretion.7 

These people require more support than others in the form of fructose that buffers against hypoglycemia and helps to moderate blood glucose levels, extra fat and protein with meals to slow the absorption of nutrients, more frequent meals, etc.


References

1.        Jung, R. T., Shetty, P. S., James, W. P., Barrand, M. A. & Callingham, B. A. Reduced thermogenesis in obesity. Nature 279, 322–3 (1979).
2.        Golay, A. et al. Glucose-induced thermogenesis in nondiabetic and diabetic obese subjects. Diabetes 31, 1023–8 (1982).
3.        Acheson, K., Jéquier, E. & Wahren, J. Influence of beta-adrenergic blockade on glucose-induced thermogenesis in man. The Journal of clinical investigation 72, 981–6 (1983).
4.        De Pergola, G., Giorgino, F., Benigno, R., Guida, P. & Giorgino, R. Independent influence of insulin, catecholamines, and thyroid hormones on metabolic syndrome. Obesity (Silver Spring, Md.) 16, 2405–11 (2008).
5.        Young, J. B., Weiss, J. & Boufath, N. Effects of dietary monosaccharides on sympathetic nervous system activity in adipose tissues of male rats. Diabetes 53, 1271–8 (2004).
6.        Wang, D. D. et al. The Effects of Fructose Intake on Serum Uric Acid Vary among Controlled Dietary Trials 1 – 4. (2012).doi:10.3945/jn.111.151951.kidney
7.        Ahrén, B. & Lundquist, I. Effects of alpha-adrenoceptor blockade by phentolamine on basal and stimulated insulin secretion in the mouse. Acta physiologica Scandinavica 125, 211–7 (1985).



42 comments:

  1. So we should have epidemiology showing that people who consume most fructose or sucrose as % calories have lower BMI by now? Or at least, weigh no more than people on say isocaloric Mediterranean or Atkins diets. Negative data would be enough to make this argument plausible.

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    1. Good point George. I wrote this one pretty quickly so I didn't do additional research for it.

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    2. This fructose MAD may explain why fructose and BMI don't line up as dramatically as we might expect. Humans have very divergent glycemic and insulin responses to sugars and starches (GI tables are just averages). What if some get fat, some just get MAD, so the stats even out? With perhaps omega 6:3 as one the deciders.

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  2. Regarding 1#: Adequate amounts of fructose alone will cause endotoxemia in lab mice. But sucrose or fru/glu won't. Nor does it seem Orange juice will either.

    The basis for most the anti-fructose studies lays on the pure-fructose aspect, which is not very realistic or context-sensitive. It is interesting to me though, that endotoxemia can cause the complete metabolic syndrome, and probably more.

    Mice eating sucrose fine:
    http://jn.nutrition.org/content/3/1/61.full.pdf+html
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1275514/pdf/biochemj00921-0130.pdf


    Germ-free mice protected from obesity on a 'western high fat high sugar' diet: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1764762/

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    1. Great thanks for these links. Indeed, I think that the LPS raising effect of pure fructose stems from its poor digestion in the jejunum.

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    2. This is widely neglected phenomenon in the fructose debate. Isolated fructose, or excess frutose, is poorly absorbed. This is the second reason (in addition to DNL) why fructose has such a low GI.

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    3. This is the study Dr. Lustig uses in his book to support the idea that fructose increases LPS levels:

      http://jn.nutrition.org/content/138/8/1452.full.pdf

      Circumstantial evidence to say the least.

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  3. WOW. I cannot believe my eyes. Paul REALLY said #3 about thermogenesis? So protein is bad then, eh? How about coconut and MCT oil? {{shakes head}}

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    1. Evelyn that was my thoughts exactly!!!!! LOL!

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    2. http://www.humansarenotbroken.com/perfect-health-diet-q-a-with-paul-jaminet/

      "Kim seems to think it’s a good sign that “fructose ingestion induces thermogenesis”. However, in my view thermogenesis is a bad sign. It implies the presence of an energy excess (or a toxic macronutrient) which had to be disposed of. If you were providing only what the body needed, then your body would be quite happy to take in a minimum of calories and waste nothing. This is a general observation, I think the excess calorie utilization on some diets that has been dubbed “metabolic advantage” is really a health disadvantage; and the healthiest diet is the diet that eliminates hunger with the smallest calorie intake."

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    3. Just finished speed reading the new PHD. (I skipped the supplement thing). He STILL cites Lustig's YouTube video on Fructose (complete with page views). That is no way to be taken seriously on the topic IMO. Many logical flaws. "Cons" for fructose are "pros" for other things :(

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    4. Some one told me that Lustig compares the metabolism and effects of fructose/sucrose to ethanol; as if fructose/sucrose could lead to cirrhosis like ethanol does. It's ironic since fructose softens the damages caused by ethanol in the liver in part by accelerating its detoxification. . . .

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    5. Yes, it's basically "pick your poison".

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  4. There have already been sucrose versus glucose (starch) studies performed which contradict your thought experiment.

    Calories, rather than the type of saccharide consumed, determined weight gain.

    Look for the study "metabolic and behavioral effects of a high-sucrose diet during weight loss". It lasted 6 weeks, isocaloric replacement of about 125 grams of sucrose and starch. By your calculations the sucrose group should have experienced roughly half a pound of extra weight loss, but no such advantage was seen.

    If sucrose is better for promoting satiety that's one thing, but the evidence that it possesses some metabolic advantage is sorely lacking.

    I agree that short term responses to meals can be informative, but not in this case.

    -M Scott

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    1. Hi Scott, I think the point was lost in that response due to the thought experiment; considering the means by which fructose exerts its thermogenic effects, fructose's effect on increasing EE is not necessarily a bad sign or a sign of toxicity. Comparing (1) starches to fructose or sucrose or (2) fruit to glucose or sucrose is not as practical as comparing (3) glucose to fructose or sucrose or (4) starches to fruit. The study you alluded to did just that, compared sucrose to starches, and lasted 6 weeks (hence, the offhand year long thought experiment). Energy balance over time, not calories ingested, determine weight gain.

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  5. I agree with Paul. It's probably only an "advantage" if it's desirable for some other reason, like enjoying the therapeutic effects of ketones, or rapidly oxidizing fat reserves. Otherwise, it's all just friction, isn't it?

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    1. Exactly. I think there's something to be said about maintaining a high body temperature. Because uric acid was brought up, as to gout, the body temperature determines the pattern of uric acid crystal deposition: Lower body temperatures favor uric acid crystal deposition, whereas higher body temperatures discourage it. Accordingly the commonest sites of gout are the extremities, such as joints of the big toe, hands, wrists, and outer ear (pinna).

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    2. interesting! Is it a coincidence that the ketotic diets evolved in the Arctic? Thermogenesis being efficient for temperature control in colder environments perhaps.

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  6. "I posit that the healthiest diet is the diet that allows us to eat the most, while minimizing the likelihood of gaining weight."

    Restated: "Three cheers for bulimia!"

    Seriously though this makes little sense.

    How is eating more than is required for optimal health & performance anything but a waste of time, money and environmental resources?


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    1. I don't like how you phrased that last question or twisted my meaning; bulimia is no joke. Simply put, a high rate of energy generation is synonymous with 'optimal health & performance."

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    2. "Simply put, a high rate of energy generation is synonymous with 'optimal health & performance."

      If that is on demand than yes, but constantly consuming energy that is not put use is rather well wasteful.

      Which brings me back to my original point which you conveniently ignored:

      How is eating more than is required for optimal health & performance anything but a waste of time, money and environmental resources?

      "I don't like how you phrased that last question or twisted my meaning; bulimia is no joke."

      Uh huh. Sanctimony can make us feel so good about ourselves.


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    3. " Which brings me back to my original point which you conveniently ignored:

      How is eating more than is required for optimal health & performance anything but a waste of time, money and environmental resources?"


      Sorry it wasn't my intention to conveniently ignore your question.

      Anyway, you're arguing apples to oranges. Of course eating no more than what's absolutely needed at the moment for optimal health and performance is ideal (Doesn't this go without saying?) But what is your conception of optimal health? For that matter, what is your conception of bodily waste? What is your conception of nutrient effects on metabolism, and the subsequent subtle, yet important, physical changes to cells and the surrounding medium?

      The point was that Dr. Jaminet seems to think that the smallest amount of food that terminates hunger is ideal. A diet filled with fat and protein will terminate hunger, but this isn't necessarily optimal, as Dr. Jaminet seems to think in my opinion. Taking some cocaine with your meals, by raising NE in synapses will terminate hunger, too, leading to fewer calories eaten.


      "Uh huh. Sanctimony can make us feel so good about ourselves."

      ??

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    4. I did an N=1 experiment with cocaine once, didn't end well.

      Great Blog Andrew

      I'm reading "The relation of alimentation and disease' on google books. Interesting!

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    5. Hi coconutz, thanks much. I agree, it's an interesting book; glad you're reading it.

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    6. @Andrew
      I agree with Paul that the optimal diet would eliminate hunger with the smallest amount of input.

      But I also agree with the sentence that proceeded what you quoted:
      "If you were providing only what the body needed, then your body would be quite happy to take in a minimum of calories and waste nothing."

      Which sounds a lot like this:
      "Of course eating no more than what's absolutely needed at the moment for optimal health and performance is ideal (Doesn't this go without saying?)"

      Hmm so you agree with Paul. Good to know.

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    7. I don't agree with Paul. In other words, I don't think that the healthiest diet is the one that terminates hunger with the smallest amount of food. Again, what is your conception of keeping the body 'quite happy' and what is your conception of 'waste?' I don't think you can consider what you're asking me in a vacuum, which is what you're doing.

      I also don't think my quote, which again, goes without saying, is the same as Paul's.

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    8. "I also don't think my quote, which again, goes without saying, is the same as Paul's."

      How are yours and Paul's statements materially different?

      Let's mash them up and find out!

      "If you were providing only what the body [absolutely needs at the moment for optimal health and performance] then your body would be quite happy to take in a minimum of calories and waste nothing."

      "Of course eating no more than what's absolutely [needed] is ideal (Doesn't this go without saying?)"

      Again how are these statements different?

      Did Paul fail by not detailing what he means by "needed"?


      Regarding waste I go back to your original statement:
      "I posit that the healthiest diet is the diet that allows us to eat the most, while minimizing the likelihood of gaining weight."

      I proffered that this diet was a waste of time, money and environmental resources.

      Explain to me how eating more than you need to satisfy hunger is not a waste of those things.

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  7. I actually had endotoxemia -- after I stopped eating safe starches and switched to fruit, the difference was like night and day.

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  8. Andrew,

    I'm trying to get to the bottom of whether high-dose iodine does in fact suppress the thyroid. I know that this is commonly believed, and more specifically, I know that Peat and his followers make this claim (and reference at least one study).

    But I cannot avoid giving weight to the clinical experience of the "iodine doctors": Abraham, Brownstein, Flechas, Derry, et al. They argue emphatically that high-dose iodine (50mg/day and up) does not suppress thyroid if it is accompanied with sufficient selenium and other companion nutrients. Indeed, they use high-dose iodine to TREAT hypothyroidism.

    Might these doctors be right that the case against high-dose iodine is rooted in old prejudices and misunderstandings? Or is there really compelling evidence to the contrary?

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    1. Although I mostly agree with Ray Peat, I believe that he is wrong about certain things, such as iodine. When the iodine content of the American diet was higher(because of iodine in bread and milk for example) the incidence of hypothyroidism was lower. I know older people who have taken drops of Lugol's solution every day for decades and they are in great health.

      If you notice on some of the forums dedicated to Ray Peat's philosophies, many of the people are still having problems with weight, body temperature and other symptoms of hypothyroidism even though they take thyroid hormones and other Peat-recommended supplements and are following a strict Peat-style diet.

      In one interview, Ray Peat said that in certain parts of the world, iodine deficiency is the cause of hypothyroidism, but in the US, iodine deficiency is not the cause of hypothyroidism. That makes no sense at all. So a hypothyroid person in China can be treated with iodine, but a hypothyroid person in America needs thyroid supplement?

      Ray Peat just ASSUMES that all Americans are receiving enough iodine. Never mind that Americans ingest a lot of fluoride and bromine which can displace iodine in the body. And bread and mass-distributed milk are no longer good sources of iodine. Also, iodine is essential for all the cells in the body, not just the thyroid. But Ray Peat believes that the iodine doctors like Brownstein are just trying to make money by scaring people about bromine. I find it interesting that Ray Peat thinks it is safe to ingest calcium and sodium in quantities well above the RDA, yet he accepts that the RDA for iodine is more than adequate. How does he explain the healthy people in cultures that ingest very little calcium and no milk?

      It is quite disturbing how many people accept everything Ray Peat says without question. No one person can be right about everything. It is simply not possible for Ray Peat to be an expert in every area of health and nutrition.

      I myself follow a Peat-style diet (mostly fruit, lots of milk,cheese, no PUFA) but I also take about 12-25mg of iodine a few days a week. After months of following a strict Peat style diet,including recommended supplements and progesterone, I still was not getting results. Adding iodine made a remarkable difference. It helped me, whereas pregnenolone and progesterone, which Ray Peat thinks are so wonderful, did not. I think it is a lot safer to add a few milligrams of iodine to the diet than to play around with thyroid hormone as many Peat followers do.

      I think Ray Peat is right about PUFA and estrogen being harmful. But even the sugar vs starch debate is confusing. I myself gain weight with starches, but I know people who eat lots of starches and no fruit or sugar and are very slim. The Japanese eat a lot of starches and they don't have the weight problems that Americans do. They also live longer than Americans. I wonder if the iodine from the fish and seaweed that they eat has something to do with that? Maybe high intake of iodine can increase the metabolism.

      And no one bother mentioning Hashimoto's disease as the curse of high iodine intake in Japan. The disease is named after the Japanese doctor who described the condition while working in Germany. If iodine can be blamed for Hashimoto's, then calcium can be blamed for osteoporosis since the countries with the highest intake of calcium (from milk and cheese) also have the highest rate of osteoporosis. Iodine does not cause thyroid problems any more than milk causes osteoporosis.

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    2. Also, like iodine, vitamin K and vitamin D were nutrients that we were warned about in the past. They were supposedly needed in only very small quantities and would cause horrible things to happen if any amount even slightly above the RDA was ingested. Now we understand that most people are deficient in these nutrients and large amounts are helpful in treating certain conditions, like osteoporosis and autoimmune disorder.

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    3. I don't know what Dr. Peat's stance on iodine is, but high doses of iodine is used to inhibit the thyroid gland when the production of thyroid hormone is excessive (e.g., thyroid tumors) in clinical practice. It's also used to prepare hyperthyroid subjects for surgical resection of the thyroid gland, which is part and parcel to the treatment of "thyroid storms." Diets deficient in iodine decrease thyroid hormone production, but the addition of iodine to salts has largely taken care of our needs for this trace mineral, which, unlike calcium and sodium, is needed in extremely small amounts. There's also quite a bit of recycling of iodine by the thyroid gland (pmid: 11573132).

      For perspective, about 100 nmol of T4 are produced per day, and so conservatively about 500 nmol of iodine is needed per day; this is equivalent to only 70 micrograms of iodine (The last time I checked, the incidence of simple, non-toxic goiters [once called Derbyshire neck] in the US has been largely eradicated.)

      The Japanese also eat soy, a goitrogen, so it's conceivable that their higher intake of sea vegetables balances this out. Thus the need for iodine probably varies among populations, but even still, the range of requirements for it is very small in comparison to other nutrients.

      Issues related to hypothyroidism in the US stem from other problems--not simply iodine deficiency, as is the case in less developed parts of the world.

      Indeed, the habit of drinking milk into adulthood, with some exceptions (like indigenous African pastoralists and Northern Europeans), is an aberrant practice. But the protein and calcium in milk is highly protective against osteoporosis--regardless of whether your ancestors drank milk or not. The upper limit is established by the RDA but, in the absence of kidney diseases, in which case, all minerals become problematic, higher intakes are generally considered safe (I discuss this issue in my post on calcium).

      I don't think high intakes of iodine cause Hashimoto's thyroiditis; they only aggravate it.

      Sorry I don't know who Dr. Brownstein is, but I'd be happy to read his work.

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    4. I'm the same "Anonymous" from the initial iodine post.

      Another,

      Thank you for your response! Learning that iodine made such a difference for you (especially when pregnenolone and progesterone did not) is a more valuable tidbit than all the theorizing in the world.

      Andrew,

      Thank you, too. If you are interested in reading the work of the "iodine doctors" (and I would recommend starting with Abraham, not Brownstein), see

      www.optimox.com/pics/Iodine/opt_Research_I.shtml

      In these papers, Abraham addresses directly most of the points you made in your response.

      Also, a fair overview of the high-dose iodine debate can be found at

      www.westonaprice.org/metabolic-disorders/the-great-iodine-debate

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    5. Thanks for these links; they seem to be direct source material for the points summarized by "Another."

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  9. Iodine was added to salt around 1924, at the request of government initiatives, due to the growing need for regulation of iodine deficiency disorders. In the 1920′s era in the United States, the Great Lakes and Pacific Northwest region of the country experienced high incidences of goiter (a common thyroid-malfunction-based condition). This was because their soil levels were extremely low in iodine, and people weren’t eating iodine rich foods
    http://www.globalhealingcenter.com/natural-health/iodine-in-salt/

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  10. Regarding iodine and assuming the inhibitory affects of fluoride and bromine - wouldn't chloride block iodine as well? As in ingesting iodine with iodized salt?

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  11. I've been worrying a bit about my daily 50mg of iodoral. Although it can be hard to comprehend the scientific language here, I feel I can glean a little of the push and pull as regards taking iodine. Medically I'm not sure why I need so much but when taking into account the diet one could sort of see that if you don't eat iodized salt, eat a few poorly cooked goitrogen foods, and get your veggies from unknown or poorly mineralized soil then higher doses of iodine supplement could just be bringing you to a neutral state. Anyway, I'm looking forward to the results of an iodine loading test so I can reduce my dose if I'm all topped up:)

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  12. As someone who has been plagued by reactive hypoglycemia for decades, I can confirm that the single food that most effectively brings my blood sugar back in check is a whole apple, or two. As we know, these "bags of sugar" are loaded with fructose in about a 2:1 fructose:glucose ratio.

    I think I'm going to try to eat one with every meal instead of just as a failsafe when shit goes awry and see what happens.

    Thanks for the post, Andrew.

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  13. "But fructose (and sucrose) is less likely to lead to an increase in body fat than glucose (and starch) because, as compared to glucose, the ingestion of fructose, as a conservative estimate, leads to a 10-fold greater increase in energy expenditure than glucose does for hours afterwards."

    Huh? Is this only if you ignore the other effects of fructose consumption? Like reduced fat-oxidation and decreased insulin sensitivity? I would be interested to hear your take on this stdudy: "Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans"

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