Thursday, June 21, 2012

Saturated Fat Kills Gut Bacteria & Modifies Genes in the Distal Small Intestine - Another Reason Why We Get Fat? Plus: Bacteria, Fiber, SCFA, GLP-1 & PYY Revisited

Image 1: Bacteria, there are >100 trillion of them right inside of your digestive track, you can hardly know them all and scientists do neither - the only thing we are beginning to understand, though, is that it may be a good idea to get them to know at least somewhat better ;-)
I guess some of you have already noticed that I was (and probably am now, again) somewhat behind, as far as answering your questions, comments an wise remarks are concerned. Actually it is still more of a coincidence that today's SuppVersity news, which, as you see is not an Adelfo Cerame post (don't forget to keep the fingers crossed for him! This is his weekend!), could actually be interpreted as my somewhat lengthy response to a comment from Vincente on the effects of GLP-1 on chocolate preference in rats and an interesting hypothesis of his, on how this could all relate to my previous post on the fat burning effects of GLP-1 ("Eat More, Burn More and Lose Fat Like on Crack with GLP-1!?"). What, that was Vincente's reasoning, what, if those obese individuals had just messed up their gut bacteria an would lack those beneficial bacteria, which convert the fiber and resistant starch that makes it through your small intestine, right down into your long one to short chain fatty acids?

Does obesity come from within?

I guess by now some of you may already be asking themselves, where all that relates to GLP-1 and eating more, burning more and losing fat like on crack. Well, the missing link if you will is actually not a link, but rather a receptor - the free fatty acid receptor, FFR, which "sniffs" the presence of the short chain fatty acids and triggers the release of GLP-1 and PYY. Those two incretin hormones, of which researchers have found within the past 10 years or so that they are way more than mere "satiety signals. Several research studies in rodents have shown that the anti-obesogenic effects of GLP-1 and PYY are if at all, only partly mediated by reductions in food intake, yet mostly via complex downstream effects on total energy expenditure, glucose and fatty acid oxidation.

Contrary to exogenously administered GLP-1, which is actually being used in the treatment of diabetes an the metabolic syndrome, the in-vivo data from rodent studies, which suggests that high fiber diets protects those little critters from diet induced obesity (Aziz. 2008; Shen. 2008; Zhou. 2008) have, as Robertson et al. pointed out only recently, not yet been confirmed in humans trials (Robertson. 2012). Moreover, the latest results from the Merck Reserach Lab show, contrary to previous evidence from the Cambridge Institute for Medical Research (Tolhorst. 2012), that even our current assumption with respect to the underlying mechanism, could at least be incomplete (Lin. 2012). This does not mean that the short chain fatty acids would not produce the desired increase in GLP-1 nad PYY, but rather that their effects are not solely mediated by  the aforementioned free fatty acid receptor in the gut.

Let's make things even more complicated and bring some long chain fatty acids to the table!

What is yet self-evident though is that the way GLP-1 and PYY modulate energy utilization punches yet another huge hole in the prostrated "calories in vs. calories out hypothesis", one that has little to nothing to o with insulin and one that acquires yet another shade of gray, when we look at the long-chain counterpart of the "bacterial excrements" the dreaded or beloved (depending on the standpoint of the individual) saturated fatty acids (SFA) and a recently published study by scientists from the Wageningen University in the Netherlands (De Wit. 2012), who investigated the long-term effects (8 week, study conducted on mice) of high fat diets with fats from different fat sources
  • palm oil - representing the saturated fatty acids,
  • olive oil - representing the mono-unsaturated fatty acids, and
  • safflower oil - representing the polyunsaturated fatty acids
on body weight gain, liver triglycerides and the whole other standard parameters and their relation changes in the gut microbiome and the amount of fat that "left" the animals undigested.
Figure 1: Fecal fat and energy loss, total energy intake and relative (to control on normal chow) liver triglycerides, oral glucose tolerance and weight gain over the 8 week study period (de Wit. 2012)
A casual look at the data in figure 1 should suffice to see that there is a profound mismatch between almost all classic features of the metabolic syndrome of which we would usually expect that they would be closely associated:
  • the rodents in the palm oil group ate the least amount of energy, excreted the greatest amount of fat and total energy in their feces and still gained the greatest amount of body weight and had the highest amount of liver triglycerides (beginning non-alcoholic fatty liver disease)
  • the rodents in the olive oil group did not consume significantly more amount of energy or excrete significantly more amount of fat / energy in their feces and still gained ~40% less body weight and did not exhibit similarly high triglyceride storage in the liver as the rodents on the saturate fat (palm oil)
  • the rodents in the safflower oil group were comparably ravenous (+20% energy intake), but although they did not excrete more energy and fat than their peers, their bosy weight gain was profoundly reduced and their liver triglycerides were better than in the "non high fat control group" and yet their glucose tolerance was not the best, but the worst of all the three groups
All that does only make sense, when a second parameter, or I should say another 100 trillion bacterial parameters come into play and the SFA induced reduction in microbial diversity and
(increased the firmicutes/bacteroidetes ratio) are accounted for, as well. those, this is at least what de Wit et al. believe are namely responsible for the complex changes in genes that regulate the fatty acid metabolism and expression of inflammatory markers, the scientists observed

Chicken or egg, cause of correlation? Or just gut optimization?

Even tde Wit et al. do yet point out that their observations do not provide significant evidence to establish a causal relationship between the bacterial changes, which are a direct result of an overflow of (selectively) antimicrobial saturated fats into the distal part of the intestine, the subsequent disturbances in the bacterial balance and (human!) gene expression in the gut and the  particularly pronounced obesogenic effects of saturated fatty acids.

You could, at least in my humble opinion, even argue that these are simply adaptive effects that ensure that the "host", in this case the rodents, "gets the most" out of his diet - after all, this is exactly what we are seeing here: A modulation of genes related to the conservation and storage of energy, such as the downregulation of the Bcmo 1 gene that predisposes to the development of obesity and non-alcoholic fatty liver disease (Hessel. 2008),  which allows for maximal energy efficiency despite greater fecal energy loss.

Conclusion? Drink safflower oil?

That these results should not be taken as an incentive to guzzle safflower oil (or drop your coconut oil for the latter) should be obvious. Just as obvious, by the way, as the realization that despite all the hoopla and my own excitement about the newly discovered importance of the gut microbiome as one of the possible contributers to the global obesity epidemic. We are understanding way too little about its interactions with its host, i.e. us, to exclude that we are not - yet again - confusing cause and effect, causation and correlation and take our gut microbiome, which is eventually nothing else than a mirror of our healthy or unhealthy lifestyle for the real deal, and try to modulate and fix the mirror image with anti-, pro- or prebiotics without working on what stands right before the mirror: The sedentary, convenience food consumer, who works to jobs and rather watches TV till late at night instead of getting his 7-8h of sleep....

  1. Aziz AA, Kenney LS, Goulet B, Abdel-Aal el-S. Dietary starch type affects body weight and glycemic control in freely fed but not energy-restricted obese rats. J Nutr. 2009 Oct;139(10):1881-9. Epub 2009 Aug 19. 
  2. Hessel S, Eichinger A, Isken A, Amengual J, Hunzelmann S, Hoeller U, Elste V,  Hunziker W, Goralczyk R, Oberhauser V, von Lintig J, Wyss A. CMO1 deficiency abolishes vitamin A production from beta-carotene and alters lipid metabolism in mice. J Biol Chem. 2007 Nov 16;282(46):33553-61.
  3. Lin HV, Frassetto A, Kowalik EJ Jr, Nawrocki AR, Lu MM, Kosinski JR, Hubert JA, Szeto D, Yao X, Forrest G, Marsh DJ. Butyrate and propionate protect against  diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms. PLoS One. 2012;7(4):e35240.
  4. Robertson MD. Dietary-resistant starch and glucose metabolism. Curr Opin Clin Nutr Metab Care. 2012 Jul;15(4):362-7. 
  5. Shen L, Keenan MJ, Martin RJ, Tulley RT, Raggio AM, McCutcheon KL, Zhou J. Dietary resistant starch increases hypothalamic POMC expression in rats. Obesity  (Silver Spring). 2009 Jan;17(1):40-5. Epub 2008 Oct 23.
  6. Tolhurst G, Heffron H, Lam YS, Parker HE, Habib AM, Diakogiannaki E, Cameron J, Grosse J, Reimann F, Gribble FM. Short-chain fatty acids stimulate glucagon-like peptide-1 secretion via the G-protein-coupled receptor FFAR2. Diabetes. 2012 Feb;61(2):364-71.
  7. Zhou J, Martin RJ, Tulley RT, Raggio AM, McCutcheon KL, Shen L, Danna SC, Tripathy S, Hegsted M, Keenan MJ. Dietary resistant starch upregulates total GLP-1 and PYY in a sustained day-long manner through fermentation in rodents. Am J Physiol Endocrinol Metab. 2008 Nov;295(5):E1160-6.
  8. de Wit NJ, Derrien M, Bosch-Vermeulen H, Oosterink E, Keshtkar S, Duval C, de Vogel-van den Bosch J, Kleerebezem M, Müller M, van der Meer R. Saturated fat stimulates obesity and hepatic steatosis and affects gut microbiota composition by an enhanced overflow of dietary fat to the distal intestine. Am J Physiol Gastrointest Liver Physiol. 2012 Jun 14.
  9. Zhou J, Martin RJ, Tulley RT, Raggio AM, McCutcheon KL, Shen L, Danna SC, Tripathy S, Hegsted M, Keenan MJ. Dietary resistant starch upregulates total GLP-1 and PYY in a sustained day-long manner through fermentation in rodents. Am J Physiol Endocrinol Metab. 2008 Nov;295(5):E1160-6. 


  1. I couldn't agree more. There are some that even argue that less needs to reach the distal gut due to increased exposure to LPS/LTA. It's interesting that they chose palm oil instead of butter oil, tallow, or coconut oil. Also, I've read before that tocotrienols have been shown to increase liver size in rats, perhaps this could be a confounder. Either way, good update on the microbiome and it's mystery. I feel we chase ghosts sometimes, but I can see how damaging an ecology may lead to ill effects as opposed to conserving it.

    1. the regular palm oil (refined as it is used in those rodent studies) is not particularly rich in tocotrienols, but in essence the message is that the potential no. of confounding factors is large and more importantly they do not ad up, but interact in a, as you say, "mysterious" way - it's much like the "Butterfly effect" with the stroke of a butterfly in the Amazonian rain forest determining your local whether ;-)

  2. Isn't the optimal dietary intake of PUFA on the order of ~4% of daily energy intake? My belief was that PUFAs are required in minimal amounts for such things as brain function and eicosanoids, and because they are highly susceptible to lipid peroxidation, they are not stored for use as energy due to potential increase in oxidative stress, as they tend to decrease bodily stores of fat-soluble antioxidants like vitamin E. Wouldn't the phenomena of increased thermogenesis and decreased storage of PUFA compared to SFA be results of the liver oxidizing excess PUFA as if it was toxic?

    Thanks Dr. Andro. Your blog is literally awesome!

    1. not automatically, or I should say indefinitely. There seems to be a "natural emergency break", when load of oxidized PUFA is increasing and the inflammation becomes exuberant the metabolic advantage of PUFAs (i.e. being easily oxidized) turns against you and causes all sides of negative downstream effects.

      That being said, I am aware of various recommendations as far as PUFA intake is concerned and none of them is scientifically legitimate - even the degree to which PUFAs are actually essential to adult human beings (at least ingested on a daily basis) is open to debate imho. That does not mean that I am with Ray Peat, as far as the "all PUFA are toxic" hypothesis is concerned, but I would like to point out that the "fat is bad" debate that was instigated in the 1970-80s was missing the point, when it turned from all fats to the bad saturated fats and the "healthy PUFAs", as the modern Western diet is by no means lacking PUFAs in general and even the claim that we need tons of additional omega-3s should be reconsidered against having a baseline level not in % but absolute on a per week and not per day basis

    2. Daily recommendations of this and that... PUFA, Omega -3s etc... What's this all about?? I mean come on, how did humans live millions of years? Did they consider all this to survive? Why now we are stressing about these points? I mean come on ... 100 years ago or past that, people didn't eat safflower, nor corn oil, nor lots of fish (depends on the region). Are you telling me that they were unhealthy. If so, human kind should have been extinguished long ago.

      Back then, they didn't knew about calories, macros, omega-3s, insulin and all the blah blah we're talking about these days. People simply ate what was available, period.

      I believe that the new eating habits we acquired lately are destroying the old one and are leading to lots of health problems, among them diabetes, obesity etc...

  3. Quote: "The sedentary, convenience food consumer, who works to jobs and rather watches TV till late at night instead of getting his 7-8h of sleep...."

    I really liked this part. Actually, it's not the fault of Fat, SFA, Insulin, Glucose ... in today's obesity epidemic! It's 200% the fault of the individual who consumes lots of food without any physical activity! In two words: portion control is no longer applicable these days.

    If i'm to compare today's eating habits with the ones from the past, ie before food abundance and desk job, TV watching, etc..., people are consuming a hilarious amount of food and calories. They eat till they're stuffed, they get fat, and later, they complain about it and try to find someone else to blame! I really hate this behavior.

    I always asked my self how come my grand parents lived long and their BMI was typical although they ate lots of saturated fats, carbs etc... The answer to that was simple: They barely ate breakfast and they "controlled" unconsciously the quantity of food they ingested during lunch and dinner. They ate treats and deserts one to two times per week (not day) and they performed a physical job.

    So what's the solution of obesity? Portion control and physical activity ... but alas, this would never happen because people are thinking with their stomach and not their head :(

    1. I guess a major problem is actually the overabundance and 24/7 availability not of food, but rather of "pleasure items" - most people don't even have an idea what HUNGER is - they only know appetite; ravenous appetite and whenever their craving for sweets is satisfied they grab a pack of chips and resensitize their pallet for the next sweet treat

  4. Just a personal anecdote about serum triglycerides:
    Highfat(mostly saturated fats from butter, coconut oil, but enough nuts and fatty fish) + lowcarb diet - 0.65 mmol/l (0.52 - 2.81)
    Moderate-low fat (50-50 saturated/monounsaturated) + moderate-high carb - 0.60 mmol/l (0.52 - 2.81)

    Not sure about portion control as there are always fat people eating almost nothing and lean ones who consuming 5-6k calories daily. My guess would be that something blunting (slowing down) our metabolism.

    1. You have luck with your genetics. I was born in a family with a history of high blood lipids. Although 'im fairly lean (10% BF), my triglycerides level is always on the high side and at some point it was very high (4 mmol/l !)

      So far, moderate-low carb diet worked for me to lower triglycerides. However, i have hard time with both losing or gaining weight. I guess my body doesn't manage triglycerides very well: so he cannot burn them easily (reason for high TG?) and cannot store them under my skin. I remember that i need to eat a lot of calories for my body to store little BF.

      I'm suspecting Thyroid disorders, although my TSH levels are in range. The reason i'm suspecting this because i read research about Hypothyroidism behind high TG and the inability to lose BF. I'm planing for a full thyroid check.

      What i want to know is, for someone like me with family high TG and cholesterol,how can i enhance fat burning. Exercise doesn't seem to do the job :( although i weight lift intensity 3 times a week + 2 HIIT sessions.

    2. I don't know, but I have my doubts that you are at 10% body fat - I have heard that too often and then people said "well, I can almost see my abs" - if you have 10% body fat you cannot "almost see them" they area simply there;

      if that is the case it is also unlikely that your thyroid would not work - I would rather take a look at chronically elevated cortisol levels.

      how is your sleep?

    3. Hi Dr. and thanks for your response.
      I'm between 10.3 and 10.7% BF according to caliper measurements (3 and 7 sites skin fold) and waist circumference measurement. My abs are visible when flexed except for a small belt at the lower part.

      Actually, i'm using "Eat Stop Eat" IF (means 2 none consecutive 24H fast) and i do count calories and carb. I have an average of -750 kcals per week, which should induce "theoretically" (although i know that this is not practical) a loss of 1.5 pound/ week but i'm way far from that. I eat clean all the time, no desert, sugar etc... and mostly complex carbs.

      I started dieting 20-05-2012 with 13.5% BF and 74.5 Kg. Today, after ~5 weeks, i'm 72.6 Kg with ~10.5% BF that's a loss of 1.9 Kg (4.2 lbs) which equals 0.84 lbs / week (not very accurate since i gained ~0.5 kg muscle). The good part is that my strength is increasing steadily and this is the first time that it's happening with me while dieting. IF seems a very good diet while on a cut, it doesn't shutdown hormones.

      What's bugging me is that i rarely feel hungry, even when i'm fasting 16 or 24h! This is always true even if i'm on a calorie surplus. I always stuff myself with food to meet calories requirements. For these requirements, i calculated a TDEE of 2350 kcal/day based on my activity level (3 days weight lifting, and on other days i have a desk job).

      My sleep isn't good most of the time. It's difficult for me to sleep and often i can't seem to enter deep sleep. Drugs like melatonin have no effect on me and ZMA worsened my sleep.

      I'm suspecting that i have a hypothyroid since it can elevate blood lipid, slow down metabolism (reason i'm not hungry?) and affect sleep etc..

    4. could be that you are already hypothyroid, but that is self induced from fasting for more than 16h... cortisol goes up, thyroid goes down, the rest as well, you are not hungry because you are driven by cortisol and catecholamines

      I guess you are also eating low carb, high protein, right? You hold water like f*** and you use pre-workouts / caffeine to get going, right?

    5. Last time i checked TSH, was 3.1 (in range max 3.5 in France, although 3.0 in US) and i was eating a normal diet (3 meals/day). However, i have read that if high cholesterol/triglycerides was measured, maximal TSH level will be 2.0 (not sure if the Dr who wrote this on her site is accurate).

      The non-hunger is something that i always had, even before starting IF. On training days, i eat high/moderate carb (~220 gr), high protein (200gr) and low/moderate? fat (~100gr). On rest days, carbs go down to 60 gr while keeping same amounts for protein/fat. I dunno if 100gr fat on workout days is high, but i'm afraid of eating more than 220 gr carbs since it will elevate my triglycerides.

      I drink a shake of 10g BCAA + 20g whey + 5g glutamine + 2g AAKG and 200mg caffeine 5min before workout. After workout, 1 bannana + 20g whey + 5g glutamine + 5g Creatine. Caffein was added recently and usually i don't drink coffee. Although sleep disorders were present before introducing coffee. If i drink tea, i do that at noon, never late in the day.

      Am i holding water duo to creatine? How can i know that? Although, i only drink creatine during workout days, which means 3 times per week.

    6. diet does not sound too bad, TSH = 3.1 = WAY TOO HIGH; I like to see that below 2.0, as well. Everything else suggests that there is something not right - especially if you are relatively lean and exercising regularly - what's your iodine intake like?

      creatine alone at 5g (I would still space that out to pre and post) should not cause water retention unless you take it with a ton of fast carbs (then those will create water retention)

      if you still retain water that would only support the high or I should say constantly elevated above a baseline cortisol hyptothesis as driving the latter will require ACTH release and that can cause water retention - do you pee several times at night?

    7. Pardon my butting in, but your last comment really sparked my interest.

      I don't go to the bathroom much during the day, but at night, I wake up every 2-3 hours to pee. It's ridiculous. I started weighing myself before I go to bed and then again in the morning just to see how much water I'm losing, and it's not unusual for me to lose 5 pounds or more just in the volume of urine I excrete throughout the night.

      I'm a layman, so I don't fully understand the implications of your comment, but does frequently urinating at night mean it is high ACTH? Or is that high cortisol? And more importantly, how do you fix it?

      I've been checked for prostate issues even and they found nothing wrong.

    8. there is nothing wrong with your prostate Chad, don't worry. And it's probably rather low cortisol...

      do you happen to sweat like a menopausal woman from time to time at night? That would also indicate adrenal problems.

      Also, any stim(ab-)use as of late?

      Possible overtraining?

      Low carb + high protein diet?

    9. I sleep pretty well actually despite getting up to pee. I wake up, go pee, and I'm right back to sleep no problem at all. No night sweats, no unexplained sweating either. Although, I do sweat a ton when I'm training. I've always been a heavy sweater though, whether I'm running or lifting weights. I once lost 7 pounds in an hour running outside on a hot day.

      The only "stim" I use is caffeine. Typically one cup of yerba mate in the morning with breakfast, and one more sometime after lunch.

      Overtraining is always a possibility for me. I believe the running mileage we're doing lately is about 25 miles a week, but we PT for at least an hour a day, and I spend a ton of time walking and standing.

      Diet is about 50-50 protein and carbs. I don't bother measuring fat intake because I am fairly confident I eat enough. I eat eggs, ground beef, and chuck roast for protein (so that's pretty fat) plus I have a tablespoon of coconut oil with eat meal, and I'll often cook with olive oil, rendered duck fat, or full fat butter.

      I definitely think I retain water though. I drink a ton of water all day, urinate very little. But then I go to bed, and I've got a full bladder within 2 hours of falling asleep.

  5. High Dr. and thanks for your replies.

    I'm not sure about iodine intake, but i use iodized salt in my food. But usualy, i don't like to add salt to my recipes if i can. I have ordered the other day Kelp supplement with iodine since i read it can regulate thyroid function.

    Since 3 weeks, i started dividing creatine between pre and post shake (2.5 g each). I don't eat carbs preworkout and i don't do either post. However, i eat around 120g carbs (complex + fruit) after my workout. I pee before sleeping and usualy i rarely pee at night, except if i drank lots of water before bed. But sometimes, i do wake up in the morning with my bladder full (with some pain).

    i'm planing on visiting my doctor to order a blood workout with TSH, T4, T3, Iodine, Manganese, Selenium, lipids etc... Should i ask him for a cortisol test? if yes, do you have any recommendations for me to follow before performing this test (other than fasted blood test). I mean, should i eat normaly (without fasting) for a week before?


    1. wait you don't add salt because it tastes too salty or because you are afraid of the NON-EXISTENT detrimental health effects? If the latter is the case you better start salting your food until they taste too salty ASAP

      don't take the kelp supplement. High dose idione will only exasperate the problem if you are not iodine deficient to begin with

      do you take a multi? or a high dose b vitamin or mineral supplements?

      as far as the blood tests are concerned, I am not sure about the adequacy of iodine serum essays and the cortisol test is pointless. That should be either a 24h urine or a 4x salivary test otherwise you have nothing but a useless snapshot and no idea what is happening in the course of the day.

      do you do carb refeeds regularly? WIth a 120g carb intake ON WORKOUT DAYs you are really on the low side of things and you said before something of >200g

    2. I add salt, but little. I don't like salty taste.

      I received my blood work test and i had this:
      FT3 : 2.58 pg/l range 2.0 - 5.0
      FT4 : 11.6 ng/l range 6.5 - 16.5
      TSH : 0.88 mUI/l range 0.39 - 3.55 !!

      I'm wondering if my lab's TSH test is accurate! Last time it was 3.03 (since 2 months)

      my FT3 seems on the low range and FT4 on the high one. i'm sure that my doctor will say that everything is ok. It's not like i want to be hypo, but i really do have hypo symptoms. What's bugging me is this fluctuation in TSH levels and the fact that it's very low this time while FT4 is high!

      Anway, i upped my carbs in workout days to 230g and on resting days i'm at 50g. should i add more carbs during rest day given that i'm trying to cut?

      By the way, currently, i'm eating the majority of my carbs after workout (185g) which is some rice/pasta/bulgur, 60g oats, 1 bannana, 1 orange and some bread. what do you think about that?

    3. TSH is low, because T4 is high. The low T3 is a sign of

      a) inflammation
      b) stress
      c) low selenium

      with a and b being essentially related, and possibly solvable by increaseing carb intake. Also on rest days by the way, I have found that this up- and down- is not really ideal for many people, try to get at least 100g of carbs on your rest days. Regardless of whether you are cutting or not - throw out some fat (or protein if you are >1.5g/kg)

      the carbs after workouts is ok, if you don't run around for hours after your workouts (in other words if you workout in the evening or at least late afternoon)

    4. forgot to mention, a, b and c lead to decreased conversion of T4 => T3

    5. Thanks again for you reply.

      I'll up carbs to 100g on rest days and i'll buy me a selenium supplement.

      I have noticed after upping carbs this week, i'm feeling better and it seems that my weight loss resumed :) I'll see this week if it'll continue.

      I have a question regarding nutrition after a HIIT session (jogging mainly): should i eat directly after the session, or wait some hours? Or can i drink for example a whey shake or simply some BCAA?

    6. In some bad cases, T4 could convert into rT3 even further worsening problems, as it antogonistic to T3. I would test it as well, though serum rT3 labs isn't available in all countries, at least certanly not in Russia. Thats why so often prescibed T4 only therapies are not really effective in hypothyroid pacients.

      I suggest you to google 'stopthethyroidmadness'.

      Also try to get selenomethionine, not elemental selenium supplemt as it not really bioavailable.

    7. Forgot to mention fluoride...

    8. rT3 raises usually when you

      a) are inflamed and / or
      b) keep throwing in more and more T4, when the problem is you don't convert

      as far as selenium is concerned you can as well eat 3-4 brazil nuts a day to get plenty of selenium (good fats and other nutrients)

      don't go overboard on the supps, or your teeth get black you hair falls out, your nails get ridges etc.

      and forget about thyroidmadness... lot's of madness there // tons of fat women who want to believe their thyroid is to blame that they cannot lose weight and hilarious advice on supplementation of this that and whatever not

      the idea is good, i.e. T4 only is not adequate for most, but the rest is off the charts

    9. lastly, when you have thyroid or adrenal problems ALWAYS EAT RIGHT AFTER ANY TYPE OF EXERCISE (and not just a protein shake; you can start with that and then start to prepare a meal)

    10. Doc, I didn't think of thyroidmadness that way. It is perfect scapegoat:
      - hypothyroidism is somewhat hard to diagnose
      - you can blame it for every single health condition
      - one pill can "solve" all your problems

      I would also suggest you to check body temperature and heart rate through the day.