Forum Replies Created
I have not looked into PCOS extensively in the past, so please take these thoughts with great criticism.
Let me start by commenting on some stuff you may have already read or are likely to read about with some searching around. Then I’ll end with some general opinions on the approach I would take. But know that ultimately your own tinkering is likely going to be needed in order to find the cure, and most out on the web are very comfortable telling others how to do things, even when their own health sucks. (I suppose I am not that much different in that sense, since I am still fighting my own battles. So, again, take these things carefully.)
Recent trials have appeared to find fairly decent success in PCOS by supplementing inositol.
The question would be, how is inositol, which is not universally considered an essential nutrient, helping hormones and/or metabolic function in PCOS women? Well, I have some thoughts. The first possibility is the obvious, and that is that inositol actually is essential in the diet, and that for whatever reason some women have a much harder time biosynthesizing a certain minimum than others and/or have increased dietary requirements for other reasons. But considering the shear quantity being used by some women and in trials, which I find to be higher than what one could get from a reasonable diet, I think the pharmacological amount is likely partly making up for something else. And that that something else is what we should be restoring.
Inositol is known to be important as a ‘second messenger’ which just means it is an essential part of certain hormonal cascades, including insulin. An inositol deficiency could therefore mean, in theory, less efficient insulin signalling and a resultant ‘resistance’. Since PCOS women are commonly insulin resistant, inositol deficiency seems to make a nice and tidy explanation. However, not all PCOS women are insulin resistant, and even massive doses of inositol does not fully cure the PCOS or insulin resistance so I have a hard time accepting that this mechanism should be considered universally applicable.
Inositol is also important as a component in phospholipids, much like choline, though not nearly as important in scale. Choline deficiency is a huge factor in fatty liver and liver dysfunction, and in animal studies going way back, both inositol and choline can alleviate the fatty liver. What is interesting is that they appear to do this via separate mechanisms. Choline is needed to help the liver escort fat and cholesterol to peripheral tissues. And inositol appears to downregulate lipogenesis in the liver, thereby lowering the need for choline (less fat is needed to escort out of the liver).
While we’re on the subject, I would like to say that both taurine and glycine (amino acids) relieve some burden on choline by moving cholesterol into the bile-synthesis pathway, as opposed to the systemic circulation pathway. Taurine and glycine have both been shown to be highly protective in high fat diets in rats and mice in alleviating metabolic stress in the liver, and in human trials in appearing to help many serum markers that have become common to track (triglycerides, LDL-c, HDL-c, fasting glucose, etc.). Glycine and taurine have both improved insulin resistance in humans, as has choline supplementation. The liver is known to be a key intermediate of the metabolism of many nutrients, so it would not be surprising to me to find out that a major systemic illness was actually liver injury as its root.
Several other dietary factors connect to this. Fructose, for instance, can be malabsorbed and can fuel bad flora growth with the resultant endotoxemia which places big time stress on the liver. Presumably, this would drain liver stores of several nutrients, including choline, glutathione, glycine, and some B vitamins like thiamine and whatever else. But eating enough glucose or starch with the fructose would alleviate this problem, since fructose is well absorbed provided one eats as much or more glucose as fructose (which was the point of this entire fructose thread initially). However, if fructose is absorbed fine, even then it will place a small drain on choline levels in the liver, since a good portion of fructose is turned into triglycerides in the liver, which then need to be exported systemically via phosphatidylcholine. This is not me saying ‘fructose is bad’, but just that fructose requires extra choline when compared with glucose. Glucose likely requires extra thiamine, since glucose is metabolized through pathways (glycolysis and pentose phosphate shunt) that rely extensively on thiamine, so we’re even. But what this means is that fructose is going to be problematic for individuals who are already low in choline. Dietary fat, too, needs choline for its processing. So, really the best diet for SPARING choline would be a starch and protein diet. But sparing choline is only so helpful. Eating choline is how one is going to make up for a deficiency, and choline is in egg yolks and organ meats. So, adding 6 egg yolks to the daily routine should help this whole thing, and lowering fat and fructose is likely not needed provided enough yolks are eaten.
Now, estrogen helps increase choline synthesis, and so men are typically the ones with insufficient choline status. It would seem possible in this case that perhaps the low estrogen, high androgen disturbance seen in PCOS is causing the inability to synthesize as much choline as is ideal, which then results in the systemic effects. Meaning that PCOS occurs first as low estrogen, which then eventually results in low choline, which then results in insulin resistance and high cortisol, which then has its own terrible effects. In this model, eating lots of egg yolks and avoiding empty sugars and fats could save one from the systemic nightmare that effects the worse-off of PCOS women, but it wouldn’t ‘cure’ the initial problem in the first place. On the other hand, it may. Even healthy women who have genetic downregulations in PEMT will be poor choline synthesizers, which could make one choline deficient independent of bad hormones to start. Then, the choline deficiency could cause the liver dysfunction and the insulin resistance and adipose dysfunction, ultimately leading to low SHBG and high androgens? Honestly, I don’t know. But I thought it might be helpful to think outloud here.
What I would recommend for everyone is to eat a well-balanced diet, high in all the known essential nutrients, while continuing to poke and prod the details of any chronic illness. Some individual may have one chronic deficiency, and another person could have a different one, but restricting the diet in any way will ultimately lead to numerous additional deficiencies which isn’t helping anything. I think a lot of people on the 180degree threads have made a go at consuming high quantities of relative junk food in an attempt to cure their problems, and I think this is a bad approach. I think eating high quantities of nutritious foods is good, but tubers, fruits, cheese, egg yolks, organ meats, shellfish, and salts beat cookies and crackers and coco-puffs any day.
I saw you asking about salt on a recent post of yours, so allow me to share some thoughts. Low blood volume is one of the major stressors on the body. The body has, as I see it, basically only two things it views as a stress: low oxygen perfusion through the brain (which could be caused by low blood volume and/or low oxygen transport via anemia and/or low CO2 since CO2 is needed for oxygen delivery to tissues) and low glucose availability for the brain. Low blood volume is a huge stressor, and low blood volume can be causes both by low sodium and also acidosis. Salt can therefore be very helpful to keep blood volume up. However, there is a caveat, and that is that acidosis produces a volume contraction. The blood has only two major anions, chloride and bicarbonate. Chloride represents the acid and bicarb the alkaline or base in the blood. When one eats lots of NaCl, a mild acidosis can result because of displaced bicarbonate. What this means practically, is that having a little NaCl can increase blood volume, but having a lot (what ‘a lot’ means depends on the person) can decrease blood volume a little. But adding some bicarbonates to the chlorides, such as a mix of NaCl and Na-bicarb can eliminate this effect. In foods, the alkaline is typically citrate and malate and from potassium. One could make their own potassium citrate by dissolving potassium bicarb in OJ, or potassium malate by dissolving potassium bicarb with apple juice or sparkling apple cider. But a balance is important. If someone used potatoes or bananas as their staple, then I would not see any reason to use sodium or potassium bicarbonate, but I would think just lots of NaCl would be good. But if someone was eaten a lot of ‘acidic-forming’ foods (grains and animal products), then adding lots of alkaline potassium PLUS NaCl would be a good approach. (As a quick aside, I would never recommend potassium chloride. Transcellular flux of intracellular ions K and Mg into cells occurs in alkaline conditions, so Na-bicarb could cause low blood K; however, acidic conditions can increase serum K and Mg, so K-Cl can dangerously elevate serum K levels. I think K-bicarb and Na-Cl are the best ways to add each, far safer than K-Cl and Na-bicarb.)
So, how about those raw vegans? In healthy people, potassium can help the kidneys retain sodium. Here’s how: increased serum potassium stimulates aldosterone secretion by the adrenals. Aldosterone is the primary ‘mineral corticoid’ in the body, which means that aldosterone is the major ‘stress’ hormone responsible for increasing blood volume. It does this via increasing sodium retention, increasing potassium excretion, and increasing acid excretion as ammonium from breaking apart amino acids. What this means is that simply having a lot of potassium could help the body retain sodium, provided that one’s adrenals are capabale of pumping fairly high amounts of aldosterone. However, in any kind of adrenal insufficiency state such as Addisons’, the adrenals are not able to pump out aldosterone in high amounts for whatever reason. I have also seen cases of thiamine deficiency causing this in rats; and aldosterone acts via stimulating methylation in the kidneys, so theoretically a deficiency of betaine and choline and methionine could cause a sort of ‘alodteronse -resistance’ in the kidneys, which could manifest as a ‘adrenal fatigue’ type thing.
Choline can be used as a methyl donor in the body to remethylate homocysteine back to methionine. Choline is turned into betaine (aka trimethylglycine, or sometimes TMG). So, a choline deficiency (which may be a piece of PCOS) would likely also manifest as a methyl donor deficiency, which could create a sort of aldosterone resistance, which could mean an inability to properly excrete acid and retain sodium, which would further increase stress hormones. Acidosis, as I have posted some about in previous posts within this thread, can have very negative effects on cortisol and other ‘stress’ hormones, which could lead to weight gain, acne, hirtuism, and whatever other terrible symptoms are common in PCOS women (and frankly many women within our society on a ‘subclinical’ level).
So, how do we approach this? Eating more choline, taurine, glycine, inositol; supplementing with enough NaCl and eating alkaline tubers and fruits as the staples; and otherwise eating a well rounded, nutrient-dense diet is, without knowing, what I would recommend.
I view a healthy diet as one that does two things:
1) provides all the essential nutrients for the body in the right ratios and amounts
2) produces a robust, healthy flora, which through mechanisms only beginning to be worked out, can mean everything for certain diseases.
Honestly, the second one is the easy one: eat foods high in resistant starch and other prebiotics, such as cooked-then-cooled potatoes and greenish bananas. Resistant starch fuels the good bugs, which produce butyrate, which itself feeds colon cells and modulates the immune system and increases Treg (regulatory T cells). For all those sports fans out there, low dose naltrexone appears to exert its anti-autoimmune effect by increasing Tregs, so butyrate is the natural way of doing this. In fact, SIBO (overgrowth of bacteria in the upper portion of the intestines) may be quickly cured by resistant starch (RS), since bacteria jump on the large RS granules but take hours to digest it. By the time they are done digesting it, the granule has long-since passed the small (upper) intestines, and is safely in the cecum (upper colon). In this way, RS effectively ‘sweeps’ the bugs down, which is presumably nice. A diet high in quickly fermenting sugars (sucrose and fructose) and small starch molecules may do the opposite by allowing the bugs to effectively climb the intestinal ladder. As long as RS is a considerable part of the diet, I don’t think sugar will give one any issues. I wish there were more clinical trials in this stuff, but there are poresently a lot of n=1 anecdotes. You can read more how to incorporate resistant starch into one’s diet by reading some of the posts at ‘Free The Animal’ and following especially ‘Tatertot’ aka Tim Steele. But long-story short, don’t eat junk food and use tubers and bananas as your staples. Don’t underestimate the power of gut health.
The first thing (getting all the essential nutrients in right ratio, etc.) is less easy, since there is far from any agreement about precisely what nutrients are essential. I have a lot of my own opinions on this, but let me just say that ratios can matter as much or more than absolute amounts, so be careful with the zinc and iron, since they can knock out copper and manganese. But following a diet with tubers and bananas, plus organ meats, yolks, yogurt/cheese, and so on to round things out, will be a good base. I personally think egg yolks are highly underrated, and I think they offer many nutrients (like choline and essential fatty acids) that will balance a tuber/fruit diet very nicely. If you need more caloric density (and may do well with extra caloric density), then try to do so with foods that are less known to cause issues to flora: so cane sugar/honey/ maple syrup not corn syrup; butter/cheese/egg yolks not vege oils. But I still think most should get their carbs from whole foods (tubers, fruit) and their fats from whole foods (yolks, cheese, organ meats, yogurt). On top of this, you can experiment around with specific supplements, but at least you’ll know you’ve got the majority of things going good with your diet.
Let me know you thoughts on all of this. This was not intended to be a full account of everything, but hopefully I have said or linked to something that you may find helpful.
I am sorry to hear about your issues. And I’d be happy to answer any questions you have, or to try to help explain things to you the best way I can so that you can hopefully solve all your problems. However, as a matter of principle, I won’t be giving out personal or contact information on the forums, since these forums are open source to all and forever. I would like to keep my personal privacy, and the only way I know how to do that is to use a pen name and to not give out personal information. I hope you can respect my position on this.
But I am patient and more than happy to communicate with you whenever you are able to write. An added benefit of doing it this way is that any golden nugget we discover together on the forums will be readable by future readers for whom the information may be a saving grace. Though I know this may make things more difficult for you in some ways, I would like to think we can make this work, if you’re up for it.
I’ll think about these things you listed and respond back soon with my thoughts.
For the K-bicarb, I would suggest starting at 1/2 tsp dissolved in 1-2 cups juice (something acidic), which will become a carbonated juice, to be drunk with each meal. OJ, apple juice, or whatever will work. Let the bubbles dissipate mostly, which should take a couple minutes after stirring the K-bicarb in. Theoretically, taking enough to bring your total ‘net endogenous acid production’ (NEAP) to zero would be ideal. This would depend on what you eat. But 1/2 tsp K-bicarb 3x daily with meals is a good guideline for most people, I think. You can always adjust from here.
I would also say that persons with adrenal insufficiency problems, which may be a big part of CFS, have a hard time expelling potassium and tend toward high potassium in the blood, even if tissue levels are low. Increasing blood potassium normally results in increased aldosterone secretion from the adrenals, which then increases potassium excretion, increases potassium uptake into tissues, and decreases sodium excretion. Thus, if one has healthy adrenals, increasing dietary potassium may actually lower sodium needs to a point. However, if one’s adrenals are not up to par and/or if ‘aldosterone resistance’ is present, then the increased blood potassium will lead to a natiuresis (a wasting of sodium into the urine), which will lower blood volume, drop blood pressure, and make you feel terrible. Independent of aldosterone, alkaline (from the bicarb) helps increase potassium uptake into cells, so K-bicarb is much less likely to cause this problem than K-chloride would. However, it should be guarded against when first supplementing with the K-bicarb. So, I recommend eating and/or drinking plenty of salt throughout the day to ensure the potassium isn’t lowering blood sodium. You can do this any way you want, including adding salt to your juice mix, or drinking salted water or whatever. But 20-40 grams of salt daily is not unreasonable for Addison’s or hypoaldosteronism patients.
As I said before, magnesium may also be needed. So, in sum, I recommend 1/2 tsp K-bicarb dissolved in at least 1 cup juice with each meal, along with ample salt and some magnesium. Ultimately experimentation is needed to sort out the ideal ratios and so on. Using sodium bicarbonate (baking soda) is a way of adding extra alkaline without the potassium, and perhaps one day you decide to do a combo of potassium and sodium bicarbonates, and other experiments. But for starters, I would recommend keeping it at potassium bicarb and sodium chloride since that is how the minerals come in foods and nature most often.
Many of your symptoms–dry, sensitive eyes; poor peripheral circulation; potential diabetes–sound like they could be Sjogren’s like issues and ‘mixed connective tissue disorder’. From some of the things I’ve read, the symptoms of Sjogren’s–which is said to be an autoimmune issue of secretory and excretory glands–are manifestations of acidosis, which is induced due to kidney damage. I would think fixing the acidosis with bicarbonate supplements could solve the eye, skin, and circulation problems. It will be interesting to see if you notice any benefit. Of course we both will be hoping for good improvement in your symptoms.
For digestion, you mentioned ox bile. Sure, try whatever. Some studies indicate taurine can glycine can both help increase bile acids, which can assist with fat digestion. But I would not assume that this will make you ‘handle’ fat better. In fact it may make you feel worse after eating fat, depending on why it is you feel worse after eating fat. If it is the absorption of endotoxin from the intestinal lumen, then any emulsifier (phospholipids from egg yolks, ox bile, or your own bile) will likely increase endotoxin influx and make your symptoms worse. But there are other possible causes of your problems, so giving ox bile a try is not a bad idea. And remember, fat needs alkaline to help digest (lipase enzymes from pancreatic excretions require an alkaline environment), so metabolic acidosis and/or too much betaine HCl with meals may severely hinder fat digestion, independent of emulsifying agents. Keep that in mind.
For your eyes and sleep, perhaps you would find a blue-light filter on your computer helpful? I know I have benefited from a blue light filter on my computer. I use F.Lux, but there are also others. I put the ‘color temperature’ usually to 2700 on bright sunny days when I have the windows open, and 1900 otherwise. Melatonin synthesis is also inhibited with blue and green light peaks, so yellowish-orangeish-redish lights before bed are likely best. A healthy person may not be bothered, but I have found it helps. It’s free and something to consider.
As for people in the Seattle area: I grew up in the Seattle area, myself. Though I don’t have any recommendations for doctors or persons to get in touch with, I would say to anyone and everyone that many (though not all) churches offer a number of supportive programs to those with disabilities and financial troubles. Catholic churches vary considerably in their help based on the assigned priest and the parishioners; Mormon churches, especially wealthy ones in upper-middle-class venues may be the best bet for getting support. Some may take offense to me saying this, but our society does not have great out-reach programs for those who, through no fault of their own, fall through the cracks, especially those with serious physical disability. The goal should always be to get back on one’s feet, and I think you can get there. But even if all goes well, it won’t happen overnight. And just surviving in the meantime, as you well know, can be near impossible. Many Mormon and Catholic churches often have support programs for persons who are not even attending or registered parishioners. Many other groups force attendance in order to get any help, which, while I understand, is less helpful for most.
Hopefully you will notice benefit soon from alkaline potassium, and perhaps soon you’ll be able to tolerate egg yolks in your diet. I am less concerned with absolute levels of fat in your diet than I am with choline-rich fats (yolks, liver) and the EFAs ARA and DHA (again, yolks and liver). While it’s not cheap, desiccated liver is a convenient option for people on the run or who can’t stand liver taste but want the health benefits of liver. It’s very low total fat but high in the phospholipids, so it may (or may not) be something you could tolerate better.
I wish you well. Stay strong. Keep in touch. I’ll be here if you have any questions for me, but I’m afraid I don’t have the answers. But perhaps you can pick up a thing here or there from me and from others and from your own experimentation and ultimately find some good answers. But I enjoy our dialogue so don’t be a stranger.
Please forgive my tendency to make typographical errors.
Honestly, your extreme reactions to fat concern me greatly, and I’m not sure how to interpret this.
As I mentioned at some point a while back to you, betaine HCl could definitely hinder fat digestion. Alkaline secretion in the intestine are needed for buffering the acid coming down from the stomach, and fat can only be properly broken apart via lipase enzymes in an alkaline environment. What this means is that if you had been and/or still are consuming many betaine HCl capsules your fat digestion could have become quite poor. Combining this with a low fat intake for some time now, and you could very well have experienced de-myelination from fat deficiency. Upon adding the fat back could give terrible sensations, which is standard for re-myelination.
Further, the acid load of the betaine HCl is worth considering. If you’re not familiar with acid/base balance as it relates to diet, consider reading these:
Basically, a net production of acid in the body which is not buffered by the kidneys at the response of various stress hormones results in massive wasting of potassium, magnesium, and calcium; lowered blood volume (which can produce the same symptoms as hyponatremia, or low sodium); and all the consequences of depleted electrolytes, including insulin resistance, poor digestion, excess histamine release, and muscle and bone loss.
Well, betaine HCl is 23.5% HCl, which means that one capsule of 648 mg betaine HCl (the NOW Foods one, for instance) has 152mg HCl. This represents about 4.3 moles of H+ ions, which is typically put into ‘equivalents’ of H+, so this would be 4.3 ‘meq’ (milli-equivalents). So, if you had taken let’s say 10 per day, then that would be ~43 meq acid, which would put you into a pretty decent acidosis. On our own, the body produces about 30-70 meq acid from normal metabolism. Ideally, your diet would perfectly balance this, so the diet would be negative 50 meq, or 50meq alkaline. It doesn’t have to be exact, but what this means is that an extra 43 meq from betaine HCl plus the body’s ~50 would result in a bout 100 meq acid needing to be buffered. Hypothyroidism (and other problems) prevents the body from properly acidifying the urine, meaning that the urine will be not acidic, but the blood is retaining acid. This is called Renal Tubular Acidosis, since an acidosis is occurring due to the renal system’s inability to excrete acid.
In any case, this could definitely create a potassium deficiency, which can, on its own, create diabetes. Fortunately, supplementing potassium in an alkaline form (such as potassium bicarbonate dissolved in OJ) can cure this fairly quickly. Something like 1/2 tsp K-bicarb with 1-2 cups OJ with each meal. This assumes you stop and/or have already stopped the betaine HCl.
Here are some paper showing/discussing rapid glucose/insulin improvement with potassium:
This may also explain your leg issues. I would add that if you are potassium deplete, you are also likely magnesium deplete. And since potassium supplementation can exacerbate magnesium problems, I would recommend supplementing some Mg-citrate or glycinate with the potassium. Something like 10-20:1 ratio K:Mg, since this is the ratio of the nutrients in most foods high in potassium.
By now, after years of restrictions of various kinds, you are likely deficient in several nutrients that could be causing a myriad of problems.
I urge you to consider ‘re-setting’ your diet to a well-rounded diet, sufficient in all known essential nutrients. Even if restricting fat makes you feel less bad for now, it is causing problems that will manifest sooner-or-later, and may already be causing a great deal of problems. Restricting an essential nutrient is never a good approach, in my opinion. I’ve done it for years myself in well-meaning attempts to help various symptoms, but it has never made anything better long-term and only ever made things worse. Any single deficiency will cause terrible symptoms eventually, and purposeful restriction of anything is likely to cause numerous deficiencies.
So, without knowing for sure which deficiencies are likely to have caused any particular symptom (though in some cases it may be obvious which deficiency is causing which symptom, it certainly isn’t always), I would say to re-focus yourself on a nutrient dense diet, expecting that an acute exacerbation of some things will occur. Then, on top of a well-rounded diet, I would recommend you consider continuing to experiment with various add-ons (‘supplements’), but no more than a couple at a time, and with the provision that you discontinue any that doesn’t seem to help after a couple weeks and that you don’t have a darn good reason for continuing. Symptoms can be caused by relative deficiencies as much as absolute, and increasing anything as the potential to induce a relative deficiency of something else, though some things less likely to do this than others.
For starters, I would suggest a well-rounded diet. Here is one suggestion (only a suggestion), which should have all the essential nutrients:
>= 4 egg yolks
~4 yellow to yellow-green bananas (more ripe reduces the prebiotic effect)
>= 4 cups OJ (with 1/4 tsp salt and 1/4-1/2 tsp potassium bicarbonate per cup)
>= 4 ounces of cheese
oatmeal (as desired)
Liver (>=2 ounces daily average)
One serving of green vegetable (spinach, kale, broccoli, whatever)
Plus whatever else you want
This would not be high fat, but it definitely has more fat than you’ve consumed in a long time. If the fat is causing your problems because of increasing endotoxin absorption, then eating good prebiotic foods (not pro-biotics, but pre-biotics) should help this. Greenish bananas, carrots, leeks are the natural foods high in good prebiotics. Oats and cold potatoes are also good. Supplementing inulin or potato starch is something some find helpful, but I would prefer whole foods to refined fiber supplements. On a personal level, eating 1 greenish banana with each meal was the thing some time ago that made a curative difference in my life-long IBS-d, and studies show that this can reduce endotoxin and ammonia, and their negative health complications.
As for the methylation thing you asked about, here are my thoughts. Most things out there on the internet or in books about health, whether from Mayo Clinic or Johns Hopkins or from ‘alternative’ health blogs and whatnot, are statements without any attempt at citing data to back up the comments. For some things that are easily searchable, I would think that is ok. But the issue I have with mainstream Big Med–where medical statements are entirely unsupported by real data, and often times completely disproved by data–is the same issue I have with most blogs. They are essentially opinion pieces. So, what does the data say on histamine and methylation, well methyl transferase enzymes are certainly involved in histamine degradation, as you can see by looking at the enzyme pathway on figure 2 of this paper:
But it is only one part of an entire pathway. The other cofactors needed for the other enzymes are copper (DAO), B2 (MAO), niacinamide (aldehyde dehydrogenase). Without these, intermediates like aldehydes can build up. Alcohol, for instance, is toxic. However, the degradation of alcohol in the liver is ethanol to aldehyde, then aldehyde to carboxylic acid. The carboxylic acid is easily excreted and is relatively nontoxic. As it is, the aldehyde is far more toxic than ethanol, and so this is what produces most of the effects. Persons with low levels of aldehyde dehydrogenase (AD), whether genetic or due to niacin or thiamine deficiency will have symptoms, most of which look a lot like ‘histamine’ excess problems. Molybdenum is also important for aldehyde metabolism.
So, when someone starts taking methyl donors and has problems, my thought is that something else in the pathway is now the new rate-limiter, and that needs to be fixed, not that someone has ‘methylation excess’. I would think B2, B3, copper, and molybdenum must be supplemented. I would also think potassium potentially, since kick-starting an important pathway may kick-start cell division which requires the intracellular ions, most notably potassium. Anecdotally, potassium has helped some people when they kick start methylation.
Now genetically, various SNPs can effect methylation and the surrounding enzymes, such as CBS (trans-sulfuration) and so on, which could certainly make one person require a higher amount of one nutrient compared to another person. But, I don’t believe methylation could ever be in excess. Methyl donors only come from three places: methionine itself; betaine (through choline or just as betaine); or glycine transferring its methyl group upon catabolism to folate to produce methylfolate. Folate and B12 are just cofactors, and they have nothing to do with methylation excess.
So, methionine, betaine/choline, and glycine are all nutrients that must be looked at. Methionine, it is very clear, has close to zero toxicity within a reasonable range of what could be gotten from food AS LONG AS enough glycine, B6 and B2, molybdenum, and alkaline are present, since glycine and B6 are needed to clear Met out of the methyl cycle through trans-sulfuration. B2 just activates B6. Molybdenum is needed to handle sulfite creation in the catabolism of sulfurous aminos, and since some of met and cys can be catabolized to sulfuric acid, extra bicarb will be needed to buffer this. Betaine and choline have such low toxicity, they are both considered very safe in high doses; my only concern on them would be their effect on the flora. And glycine appears all good and potentially a must-have supplement. So, I don’t buy-in to a true ‘methylation excess’, outside of precipitating a relative deficiency in something else that was already deficient but not noticed. I suppose the term ‘over-methylation’ could be used to describe symptoms upon increasing methylation pathways, which then implies deficiencies in something else. But I’m afraid many out there use ‘over-methylation’ to actually refer to methylation excess. Maybe I have missed something, but as of now I really don’t think that is possible outside of relative deficiencies.
There is more that could be said in terms of methylation, but that it my jist.
Dan, I may have left some things unanswered. I did not mean to do that, but I wanted to make special mention of fat metabolism and glucose control since that is what may be your biggest issue symptomatically.
I urge you to consider potassium bicarb supplementation, discontinuing betaine HCl (using anhydrous Trimethylglycine would be fine and potentially even good since it can partly makeup for deficient choline, but just not with the HCl), and adding egg yolks, liver, and some prebiotics to your diet. I am sorry your leg symptoms are so bad, but continuing to restrict choline and essential fatty acids (arachidonic and DHA, both of which are found in egg yolks and liver) is not going to end well.
Yes, I definitely remember our conversations earlier this year. In fact, it was some of your comments that got me to look more into thiamine, and I’ve read a lot of goodies since then!
But I’m definitely sorry to hear that things are not better for you!
Here are some thoughts. Stasis dermatitis is common in diabetics (well, relatively common), and the tingling sensation you describe in your legs is a documented feature of the poor venous flow. However, I’m not sure how or why fat would be related to this, outside of the possibility that the dietary fat is increasing the absorbed endotoxins from the GI tract (which it does, but usually isn’t a problem), and that this is exacerbating your inflammatory reaction in your legs.
Do you ever eat egg yolks? Or liver? Phospholipids (which make up a considerable portion of the fat in organ meats and yolks) are absorbed a bit different than dietary triglycerides (most dietary fats). Besides the fact the deficiencies in choline can be a big problem (choline is associated with phospholipids in liver and yolks), it might be diagnostic to see if you had lessened or worsened reactions from eating egg yolks instead of other fat for a meal or two. But to be honest, I really don’t have any knowledge on venous problems.
In terms of the lipid and A1C issues, I have some thoughts. First, for the A1C issues. A1C is just a marker of the amount of glycation on heme. So, the number will go up with high glucose levels, but it will also go up with many forms of anemia. It is important to note that in iron deficiency anemia (or in copper deficiency anemia, or potentially even molybdenum deficiency), the heme in blood cells is degraded more slowly (because our body doesn’t have enough iron to replace it), and this allows the heme to collect glycation sugars to a greater extent. Thus, without knowing fasting glucose and/or insulin, or having a 2-hour OGTT (oral glucose tolerance test), it would be difficult to interpret the A1C. I know most doctors are more than willing to claim a high A1C as indicative of diabetes without further testing, but that’s not accurate. And I’m not saying to go get more tests done, I’m just saying more would be needed for proper interpretation (and perhaps you already have these done).
For lipids, fructose certainly can increase triglycerides, because fasting triglycerides are a marker of how much fat the liver is synthesizing de novo. The more dietary fructose and the less dietary fat, the more de novo fat synthesized. This is not a problem in and of itself, but it certainly does increase choline requirements and it may indicate overall fat deficiency (your liver is making more fat because the body needs it). This is obliviously not easy to solve if fat worsens your symptoms. But the good news is that fructose can provide the substrates for your liver to make fat (whereas glucose doesn’t as much), so if you must consume lower fat, then having higher sugar is better than higher starch, in my opinion. Now, copper is interesting here, since copper deficiency causes an increase in the amount of fat synthesized in the liver, both triglycerides and cholesterol. I don’t know if the amount of extra lipid material is excessive in copper deficiency, or if copper deficiency somehow increase the peripheral need for fat which is why the liver is making it. But either way, increased LDL-c and/or triglycerides, especially when an anemia is present and/or neurological problems exist, may be very indicative of a long-standing copper deficiency.
Thanks for the collagen and fructose links. Fructose does increase, at least in a test tube, glycation to a greater extent than glucose. But alpha lipoic acid has been studied to increase glutathione and decrease oxidative stress, and copper deficiency causes increased oxidative stress. So, again, I think a good chunk of this is just the same ole? fructose causes copper deficiency, which interestingly may be much worse in men than women. Notice how the one study you showed me shows how men are more affected by fructose in terms of collagen crosslinking. Well, check out the last 2 links here that shows males worse off with copper deficiency than females (rats, that is).
What concerns me the most about your symptoms are the neurological ones. Eye sight, for instance, is temperamental and not easily restored if something goes wrong. Sure, diabetes could cause problems relating to eye sight, but so can deficiencies in choline, copper, B12, protein, zinc, A, D, B2, the essential fatty acids (ARA and DHA; both in liver and pastured egg yolks; ARA in conventional yolks, and DHA in fish). There may be a variety of other things that could cause vision problems too, and electrolyte imbalances can create temporary issues. But if you’ve been avoiding fat for some time, than it could be that you are deficient in vitamins A, D, K2, E; ARA, DHA; and choline/phospholipids. Eating at least few yolks per day, plus the extra vitamin A and D would be something good to do right now, I would think, even as you works everything else out. Perhaps experimenting with copper and/or some other things little by little may help you tease out what is going on. That ‘balanced’ zinc/copper supp you mentioned, what is the ratio on that? I think most are too far in favor of zinc. But something like 10-15mg zinc and 3-5mg copper should be ok as a supplement, I would think. I know ratios of 10:1 to 15:1 Zn:Cu are recommended, but I think lower ratios are ideal (perhaps 5:1), especially when phytic acid foods (grains, legumes, seeds, nuts) are not consumed, since phytates inhibit zinc absorption while doing little or nothing to copper.
Also, I would ignore any bashing you read or hear on copper on the internet. It’s misplaced. Copper levels in the blood increase in times of acute or chronic illness, much like zinc and iron decrease. These are all called ?acute phase reactants?, because their levels change in acute (or chronic) inflammatory conditions. C-Reactive Protein is another acute phase reactant, and since it elevates in many instances of illness, it is used as a marker for disease severity. Serum copper could be used the same way, as a marker of illness severity, but that does not mean one with elevated serum copper is ?overloaded? with copper any more than someone with elevated C-reactive protein is overloaded with the letter ?C? because of eating too much alphabet soup. Severe copper deficiency will lower blood neutrophils (neutropenia) and could cause anemias of all types (with low, mid, or high MCV and MCH). There are many ?clues? of copper deficiency in a blood test, but serum copper itself, is not usually one of them. I think supplementing 3-6mg copper per day (in divided doses) and judging your health response is likely the best way to determine copper status, but you can stop at any time if you don’t think it is going well. Copper could theoretically increases the requirement of molybdenum, so supplementing some molybdenum with copper may not be a bad idea (I would suggest something like a 10:1 ratio Cu:Mo; or 3mg Cu with 250 mcg Mo). But go by feel.
In terms of diabetes and glucose control, deficiencies in potassium, thiamine, and magnesium would all causes an inability to process glucose through glycolysis; and diseases with wasting of potassium and magnesium (such as hyperaldosteronism) always causes a worsening of glucose control, while hypoaldosteronism can actually causes life-threatening insulin sensitivity and low glucose. But if you’re eating lots of fruits I don’t think potassium or magnesium would be a problem. It’s the refined sugars and starches that could be problematic from a potassium/magnesium standpoint (and a copper point of view), since they are void of these nutrients, but require them for proper processing. So, again, this is where fruits and tubers should be fine as staples, while refined sugars better in moderation or not at all. In cases where, let ‘s say cane sugar for example, are tolerated better than fruit, I would recommend supplementing alkaline salts of potassium and magnesium (citrate, for example) along with the sugars, and consider supplementing thiamine somewhere in there, too. But this is just me saying don’t induce a further deficiency in something while you are playing around with finding what is already wrong.
All-in-all, it sounds to me like your body is beaten down quite a lot and that you have a long road to recovery ahead of you, even if all goes well from here on out. I wish I could wave a magic wand and cure you. I suspect you have many long-standing deficiencies, and that fixing one may produce some negative effects along with the positive, since fixing one rate-limiting reaction may causes another to be rate limiting to the point of a new set of symptoms. So, if something feels good at first, but then begins to produce undesirable effects, I wouldn’t take it as that thing being bad but that something else is now needed with it. For instance, many supposedly feel weird taking iodine, but then notice that extra chloride, selenium, B2 and B3 seem to make everything swell. And anecdotally, magnesium, potassium, and niacinamide help those with sudden increases in methyl donors.
Those are my thoughts. Let me know your own thoughts, and keep in touch either way.
I haven’t been on the site for a while, but I do get emails from continued activity, so I’m happy to respond.
There are certainly a lot of studies on fructose and its problems–not to mention the public media’s banter.
Let me post some links to several studies and then comment a bit at the end. Some of these articles have free access to the whole article. I have full access to everything I post here, unless I state otherwise. I wish I could just attach a pdf, but a web link will have to do. Some really appreciate the primary scientific references, while it burdens others. But I think it’s good to include them whenever possible.
Many of the immediately deleterious effects commonly associated with fructose are abolished if given with an antibiotic, implying that it is fructose fermentation after mal-absorption resulting in endotoxemia is causing these problems (I do not have full access to the first here):
Endotoxemia induced any number of other ways has similarly negative effects typically associated with fructose; this endotoxemia can be induced fundamentally by screwing the gut flora with high protein diets (leading to protein ‘putrefaction’, which is just fermentation but of protein instead of carbs), digestion inhibitors such as wheat that lead to increased protein putrefaction, and even high fat diets which increases absorption of the fat-soluble endotoxin once made in the intestinal lumen:
And here are a couple blog posts along these lines (the author of this blog has some perspectives I don’t fully agree with, but it has some good info, I think):
Fructose is mal-absorbed by most unless taking simultaneously with equal parts glucose (or starch glucose), as measured by hydrogen and methane breath test:
Certain ‘good’ prebiotic fibers, such as inulin, seem to induce a favorable shift in the gut flora (up to a point), which can temper the negative effects of substrates that fuel pathogenic strains:
Now, there have been some studies where inulin has reversed the endotoxemia-induced obesity in mice:
But, rats really can’t digest fat well and the fat mal-absorption leads to a deficiency of certain minerals; inulin increases colon fermentation and cecal mineral absorption, which may counter-balance the decrease in mineral absorption from the mal-absorbed fat (indicating that the reverse in health of inulin-fed rats/mice may be more to do with alleviating a nutrient deficiency than correcting gut flora directly):
Once nutrient, in particular, that I think deserves a lot of attention is copper. Copper deficiency is induced in rats and mice on a high fat and/or high sugar/fructose diet; and copper supplementation counters ALL of the effects of a high sugar, high fat diet, including obesity and metabolic syndrome and heart dysfunction:
On its own, copper deficiency causes massively increased lipogenesis and cholesterol synthesis, which would result (practically speaking) in increased triglycerides, LDL-c, and fatty liver. (I don’t have full access to the third article below). Presumably acetyl CoA substrates would worsen this, meaning that diets high in fat or fructose would worsen these effects, but not glucose or protein or starch. That being said, simply avoiding sugar and fat but not actually correcting the copper deficiency is trouble. So, I would say to keep eating fruit and fats as desired, but get copper status up if this were a problem.
Now, in humans, since we typically digest fat better than mice and rats, copper is not obliterated by high fat, and inulin doesn’t boost our mineral absorption to such a great extent. Since inulin DOES improve our bifido numbers, but does not seem to help our metabolic syndrome to as great an extent as in mice/rats, I think it is safe to assume that it may NOT be the gut flora as much as nutrient status (copper status) that is leading to obesity and the metabolic syndrome. In humans, at least in a couple case studies, copper deficiency has been induced by a high intake of fructose-containing diets, indicating that fructose (not fat) definitely does play a negative role for copper status. The question I can’t answer for right now is whether it is fructose mal-absorption or fructose as is (even in sucrose) that is increasing copper requirements.
I haven’t seen anything about fructose and collagen as in your question; but considering that copper is essential for collagen and elastin formation, anecdotal reports of fructose harming collagen may in fact be observations of fructose detrimental effect on copper status, in which case simply adding several milligrams of copper as a supplement per day should correct this. Since copper status has already been obliterated in our food system over the past 100 years, I would recommend this anyway.
(this last link shows copper deficiency induces collagen hyperproliferation due to a lack of lysyl oxidase ability, resulting in emphysema in lungs, but presumably would causes similar derangements in other tissues; in skin collagen hyperproliferation is called ‘scars’ and when the collagen is laid perpendicular to the epidermis called ‘hypotrophic scars’, such as with acne scars.)
As for tryptophan and fructose, I haven’t seen anything on that specifically, either. However, tryptophan is converted to many of the necessary amines via tryptophan hydroxylase which is a copper/iron enzyme (copper is needed for iron transport, and copper deficiency induces a brain iron deficiency, which could effect this). But copper is also needed to break down neurotransmitters histamine (diamine oxidase, aka histiminase). In fact, catecholamines, tryptophan metabolites, and histamine use many of the same enzymes for catabolism, so high dose Trp, for instance, can induce excessive blood histamine and eosinophilic myalgia. Methylation (which I often think is overrated in blogs and popular websites, and about which there is more misinformation than most topics in health, I think) can be hurt via copper deficiency, since copper is needed in one way or another for COMT and Methionine Synthase. These methylation pathways are important for many things, including amine degradation. However, since copper deficiency also leads to increased transulfuration (pulling methionine down towards glutathione and cysteine, and away from methylation, presumably because they body needs the extra antioxidant power of glutathione while copper is out), it may be that increasing methylation supplements like choline, betaine, or methyl b12 and folate would do more harm than good, as they would try to pull methionine back towards methylation and away from glutathione; I don’t know about this, but I would think copper deficiency is creating a bigger need for methionine and glycine (and perhaps a little b6), and these should be supplemented over the methyl donors per se. And copper is clearly needed for niacin synthesis from Trp, so anyone who thinks they may be deficient in copper should consider supplementing niacinamide in the meantime (maybe 50-100mg 1-3 times daily), while they also supplement copper of course.
More than likely, I have missed some key references that would make this response more thoroughly ‘a priori’. But, let me now sum things up a bit.
Fructose does clearly in both human and animal studies precipitate many metabolic disturbances, including the ones most often talked about like metabolic syndrome, fatty liver, visceral fat accumulation, and even increased blood pressure. I haven’t seen anything directly on tryptophan or collagen, per se. What studies do also show, however, is that the majority of the problems with fructose are related to the effect fructose has on gut flora and mineral absorption. In terms of postprandial (post meal) endotoxemia, simply eating fructose with equal parts glucose corrects for this, and I think that is pretty straight forward. Some white rice, oats, or even dextrose or rice syrup should all be equally effective in being able to temper fructose mal-absorption. Inulin or other prebiotics may also help temper any negative consequences of fructose (or wheat or whatever) on the gut flora; however, in humans, this effect seems to be less important than in rats with respect to metabolic syndrome and obesity, and even mineral absorption, but some individuals may find it really helps. I do not know exactly why glucose helps increase fructose absorption, but the model that has been proposed is the ‘piggy back’ model, whereby one glucose molecule helps carry fructose with it through a more readily available glucose transporter. Once absorbed, fructose WILL increase the requirement for choline, since it is a building block fro bio-synthesized triglycerides, which (like dietary fat) require extra choline for proper transport out of the liver. Glucose, whether as starch or free fructose, doesn’t do this.
So, when I originally said that simply eating more glucose with fructose is ALL ONE HAS TO DO, this was a oversimplification; I would like to amend it to say one must ensure proper absorption by eating enough glucose, but then also intake enough extra choline (and perhaps other nutrients like copper) in order to compensate for the particular pathways that fructose uses over that of glucose. This is not all bad, since different pathways require different nutrients. For instance, glucose, by increasing insulin to a greater extent, relies more on Mg, potassium, and thiamine than fructose (glucose relies on the cofactors for glycolysis to a greater extent; fructose more on the fat cofactors like choline and potentially coenzyme A from B5 and copper and cysteine).
For individuals with high triglycerides from whatever reason, I would highly recommend considering supplementation or increased intake of copper and choline (choline is high in egg yolks and liver).
Fructose, and also potentially other dietary factors (and presumably many things that are poorly digested including cellulose) may decrease absorption of certain minerals, and copper deficiency is so strongly and causally linked with fructose and high fat diets that it may just be that copper deficiency can explain many of the deleterious effects of fructose in both humans and rats. And yet, the negative consequences of fructose, at least in rats, can be corrected for with modest copper supplementation; in human,s something like 3-6mg per day I would think appropriate (copper glycinate likely better than sulfate or gluconate, in my opinion), depending on the rest of the diet. Let’s first, though, take a step back and ask the question: “is it reasonable to think that copper deficiency COULD BE responsible for modern obesity and metabolic syndrome epidemics?” The answer to this, I would think, is a resounding yes. Copper status in foodstuffs has decreased 50-70% on average, and the most copper rich foods (beef liver, for instance) nobody eats anymore. On top of that, it is not just an obesity epidemic that we have. We also have a greater increase in acne scars (collagen hyperproliferation), stretch marks (weak elastin), arthritis, and whatever else that are related to copper status. Interestingly, copper peptides (copper chloride dissolved in a hydrozlyed protein carrier) are being used for spider veins, skin, scars, and stretch marks quite successfully. And since copper deficiency clearly disturbs catecholamine and amine neurotransmitters, mindful experimentation should be considered to help correct copper deficiency, whether or nor fructose was at the root of its deficiency.
Anyhoo, those are my thoughts. I’d love to know your own thoughts if you think differently on the matter. And please forgive my no-doubt ubiquitous typos.
I thank you for your well wishes. I wish you and your wife the same!
I have mixed feelings about everything these days, and the more I learn the more I feel confident everyone is wrong, but also the less I feel confident about what is right (if anything).
Symptomatically, sauna, charcoal, cholestyramine did not help. And after about 6 months of these diligently, my urine mycotoxins results went up slightly (got a little worse; lab through Real Time Labs). On top of this, I had moved out, left behind pretty much everything except washable towels and clothes (got new beds, new shoes, dishes, etc.).
‘Refeeding’ with whatever I craved really helped for the first 3-6 months, but then I plateaued/regressed. I have since started taking a multivitamin which I think has helped. As I mentioned in my original post, I have a history of restrictive eating, most notably a 4-5 year stint with the low carb paleo thing, and I suspect I built up a few deficiencies during this time. Increased calories and carbs from refeeding precipitated the deficiency symptoms (this is common in, for instance, anorexics). Copper and thiamin (B1) and B6, in particular, tend to be lowish in the modern interpretation of the ‘paleo’ diet, and supplementing these has helped me substantially within hours. (Though it wasn’t the CURE or anything).
As for Shoemaker, I think the method is partially correct. But leaching was common in medieval medicine practices, too, and it often did more harm than good (in fact, the old english for ‘physician’ is best transliterated ‘leech’).
There’s a couple thing to keep in mind:
1) A proper ‘metabolism’ and the hormones that regulate it are also responsible to maintain excretory/detox pathways, without which junk will be accumulated. If someone becomes, for instance, hypothyroid, he/she will accumulate heavy metals, plastics, molds. These environmental toxins can worsen the health still further, but they are not the cause. Besides testing positive for mycotoxins, I also tested positive for urine arsenic. I have no known source of arsenic, so that’s when I began to think things were fishy.
2) Whether or not the initial cause of bad health is, let’s say, mold, if the result is both mold accumulation AND hypothyroidism (read: full body shutdown of any kind), then attempting to leech the mycotoxins via therapies that only encourage the body’s own excretory pathways (pathways which aren’t working well) will not work well. And in the meantime, the body’s nutrients will be leeched leading to increased likelihood of nutrient deficiencies and further metabolic shutdown.
3) Restrictive diets, in particular low carb diets, often feel great for those who have intestinal issues due to overall bad health (again, which may or may not be CAUSED by molds). But these restrictive practices may create further deficiencies and do further harm to the metabolism and body.
Take my advice with a grain of salt, but I would encourage your wife:
A) If she hasn’t already, to get official urine mycotoxins tests with Real Time Labs. A lot of symptoms ‘mimic’ mold toxicity, and I think ‘environmental mold illness’ is like ‘Lyme’ and ‘candida’, which are very serious diseases some people actually do have, but most are just thrown onto the pile because they have some odd compilation of symptoms that no doctor knows how to deal with.
Real Time Labs are THE standard for this.
If the results come back negative, consider the fact that she does not have mold toxicity. If they come back ?positive?, consider the fact that she may or may not have mold toxicity as a primary issue. Either way, don’t let her leech herself too many months in a row. I think 3 months in a row should be considered a maximum, before at least 3 months of eating and NOT using cholestyramine and whatever else.
B) As for diet, I would beg your wife to NOT engage in restricting any whole classes of foods (such as ?carbs? or ‘starches?). I would make sure she eats plenty of calories and follows her apatite. The body is designed to inform us when we have a need for a certain type of nutrient, but only if it is introduced to enough foodstuffs to be able to ?know? from where each nutrient comes.
C) Consider supplementing with a decent, non-massive-dose multivitamin to see if she may have any long-standing nutrient deficiency. I like to combine a few things:
These are just what I do and something to consider. Cholestryamine is known to leech nutrients, so she may find that it helps.
As for non-mold blood tests, I have been tested for many things at my own prerogative. Now that my insurance sucks due to the whole health care ordeal, I often use directlabs, walkin labs, and life extension blood tests. Many of my blood results have been very screwy since I got sick, and I would be glad to share with you if you ever wanted that.
This post is just a smattering of thoughts. I in no way mean to patronize you or anything. I think you should do what works. But it is good to know that many things seem to work for a while, before they then make you crash and burn. I think restrictive diets fit into this category.
I will keep this stream updated with my progress as time goes on, but at the moment I don’t seem to be worsening or improving.
Your welcome, roonitune! I hope it helps. But above all else, experiment around and find what works for you. And I would say to all recovering orthorexics/anorexics/restrictive eaters, that it would be better to error on the side of NOT restricting then the opposite. So if eating bread and milk makes many things improve but gives you a few mild symptoms, stick with it. But if symptoms are quite bad (such as receding gums, noticeable autoimmune problems, suicidal depression, etc.) then consider going away from it for a while.
For me, too many grain-based cookies and cakes and ‘junk food’ bothers me. But organic breads and oatmeal and grains doesn’t so much. And sugar-based ‘junk’ (fruit snacks, straight sucrose, candy) also doesn’t bother me. And for a while, milk (raw or pasteurized), yogurt, and ice cream bothered me, but hard cheeses and butter were fine. And then after a few months of eating what I could (and a lot of it), yogurt and ice cream were also ok. So it is an evolving process.
The ideal, of course, is to crave nothing, enjoy everything, and be able to thrive off of nearly anything.
I think over activity coupled with under eating is a big disastrous, and I’m right there with you. I spent too many years of my life working out hard and restricting in one way or another. I was very healthy all my life until rapidly, over the course of a few months, I mysteriously fell apart. A few hellish years past with me experimenting around with other ways to restrict in an attempt to find health, but I kept getting worse. It was only last summer/fall that I decided to try what I never have, which is simply eating instinctually. So far, so good; though I’m not out of the woods yet.
I wish you the best with your recovery, roonitune. It’s amazing how many of us are out there having ruined our health by following the mainstream pseudoscientific propaganda spewed out by every institutional authority known to man. The numbers keep increasing.
I think the bags under the eyes are parallel with ‘extra-vasation’ of fluid anywhere, such as when people get swollen feet on a plane or after a long day on your feet. Factors ‘causing’ and/or promoting this include:
***Weak capillaries (due to prolonged elevation of catabolic hormones, and or nutrient deficiencies)
***Immune differentiation/expansion within lymph tissue (due to dietary or air-borne toxins, often exacerbated if not outright triggered by absorbed bacterial endotoxin)
***Slowed lymphatic drainage and re-uptake of extracellular fluids (due to poor overall metabolism and/or low activity)
***5 trillion other things.
In my own experience, fasting and/or low carbing would make this go away short term, and it would come right back upon eating carbs. But the more I consistently ate carbs the better it got; and the longer I consistently went without carbs, the worse it got. So, gut flora problems, stress hormones, and so on obviously play a role.
As far as histamine, I think histamine is one player in a large cascade of things, and it is often overemphasized. That said, anit-histamines (pharmaceutical or other) often seem to help people a lot in the short term, so clearly there is something to it. Histamines are needed for the migration of immune cells out of the blood into the lymph and/or extra-cellular space, which pulls fluid with it via osmosis and results in swelling. So anti-histamines will reduce swelling and congestion (and even reduce air way constriction in an acute allergy/asthma response). But histamine is also needed for gastric acid secretion, gastric motility, and differentiation of immune cells; thus, long-term anti-histamines will screw up digestion and immune cell refinement which could lead to autoimmune conditions in the worst cases.
Of course, there is a difference between lowering ?already-excessive? levels of histamine versus lowering ‘normal levels’ of histamine. Various nutrient deficiencies and/or other hormonal imbalances can cause exaggerated histamine responses.
Some factors controlling this include:
Thiamin (vit. B1):
The point here is that everything influences everything and besides correcting nutrient deficiencies, I wouldn’t mess with anti-histamines for long term therapy. I think the increased swelling in your case is due to the digestive disagreements you are experiencing from dairy and/or gluten. You could try avoiding these for now and then re-check your response every so often. Or you could try plowing through. I personally think endotoxin and intestinal issues are not worth playing around with, so I would pick the ‘avoid now, check again later’ approach, but others have done well doing differently. But you may only be reacting to dairy OR gluten, so don’t automatically throw both out. And if you do avoid these, I would recommend MAKING SURE you get your calories and nutrients from elsewhere; many people spontaneously cut food intake restrictive diets.
And keep us updated on how it goes.
Nothing profound here, just a thought.
I wanted to mention something quick about betaine. This is not related to the HCl portion, but just the betaine. Tri-methyl-glycine (betaine) is a very strong methyl donor and taking many betaine caps could result in over-methylation especially within the context of low other b vitamins. B1, B2, B3, B6, pantothenate, and biotin, and whatever else.
It may be worthwhile experimenting going off betaine HCl and trying some apple cider vinegar caps (ACV), instead.
ACV is not as acidic as betaine HCl, but it has a decent amount of acid, and many people do well with it. But it also doesn’t have so much methylation potential! So I figured it worth an experiment.
It’s been awhile since you first posted, mommyof3inidaho, but I wanted to share a few thoughts.
First, I agree with elfman5150 about the flora being severely altered while on a paleo diet. Food with high levels of ‘prebiotics’ such as bananas, potatoes, apples, and most other tubers and fruits will help selectively feed the ‘good bugs’ and give them the opportunity to re-take their appropriate spot within the circle of life in the gut. Eating ‘junk food’ tends to feed stuff very UNselectively, which means UNTIL your good bugs are up to speed, junk food will exacerbate dysbiosis and result in any number of symptoms including what you are having. I know some people do well with PRO-biotics (supplemental bacteria), but I think ‘PRE-biotics’ (foods with specific types of fibers) are better in your case since there is no evidence that you don’t have the proper bacteria, just that you need to start feeding them after this long period of starving them. It will take months to re-establish proper flora composition.
You can read my reply to another post here for more info on this kind of thing:
Second, I think electrolytes/fluid balance have a huge impact on headaches and so on. Sodium, Potassium, and Fluid must be in proper balance. As a rule, too much sodium and/or not enough potassium can cause headaches. Too much potassium and not enough sodium can cause lethargy and/or hypothermia and/or anxiety issues. Drinking water modulates all of this by lowering both potassium and sodium in the blood, and potentially lowering potassium within cells. What I mean to say by all of this is that you may try displacing some ‘junk food’ with bananas and fruit and potatoes (increasing potassium) to see if that helps. If it is to help, you should notice it within hours to days. If it hasn’t helped within a few days, forget it.
Third, I wanted to mention nutrient deficiencies and dynamics. Carbohydrates and the resultant insulin surge stimulate the uptake of a wide variety of nutrients (potassium, b vitamins, and other stuff) INTO cells, OUT of the blood. I think paleo and other restrictive diets tend to commonly be low in certain nutrients. However, it is UPON increasing carbs that the deficiency manifests itself because only then will the blood level of these already-borderline-depleted nutrients drop (as they are shuttled into tissues). Some of the most prime culprits are potassium, magnesium, thiamin, and other B vits. You may want to try supplementing some magnesium and a decent b complex to see if that helps your headaches. Fruits and tubers should give you plenty of potassium. [As a brief albeit important aside: I’m not fond of b complexes with thiamin (B1) as ‘benfotiamine’ for refeeding deficiencies since this form is a synthetic fat soluble nutrient that does not follow the same pharmacodynamics as water-soluble thiamin. So the b complex should have B1 as Thimain HCL.]
Some supp ideas could be the following (just ideas to consider):
The latter is a full multivitamin but I like it because it has natural folate and b12 and because it has more thiamin in proportion to other B-vitamins than most supps.
I hope experimenting around with these things will help lead to the promise land. Please keep us all informed on your progress!
Rosie123, are you still going strong? It’s been a few months now, and I’m just curious how things are going for you! I hope you are well.
Thanks, codys182. I HAVE tried the toaster pastries and I am a fan!
*Costco Organic Animal Crackers (mix of palm > sunflower oil)
*Honest Chips (organic coconut oil chips; hard to find except online)
*Trader Joe’s Cats Cookies (palm oil; not organic)
*Trader Joe’s Organic Toaster Pastries (palm oil)
*Nature’s Path Organic Toaster Pastries (palm oil)
Thanks, Christinam. I have read of acid/alkaline balance–though not the particular approach you mention–but I am not in agreement with it at this time.
I personally think potassium, though important, is not a prime metabolic simulator like calcium. Let me explain.
Humans, like any carnivore or omnivore, must have a body that is metabolically flexible to be able to push through short famines without dying, but also be able to turn on the growth switch after meals to renew tissues and grow. One of the ways the body ‘senses’ this is by the flux of nutrients through the blood and hepatic (liver) circulation. If you are fasting, muscles are being broken down into muscle-meat amino acids and phosphorus and your liver is using the amino acids to make glucose and the phosphorus is mostly excreted. It would be foolish to ramp up the metabolism in a time of fasting and metabolic breakdown, so muscle meat amino acids and phosphates help signal to the body to slow the metabolism. Since potassium is mostly an INTRA-cellular ion, potassium increases in times of catabolism.
Some say too much dietary muscle meat is therefore metabolically damaging, and I agree. If a hunter-gatherer killed a buffalo, and ate of it, there would be more than an increase in muscle meat pouring in from the meal; there would also be collagen amino acids from the bones and skin cooked in the cauldron, and there would be calcium from the bone broths. There may also be carbs if the humans ate some sugar or starch along with the meat, and the pot may be seasoned with salt or cooked in sea water.
Thus, the distinguishing features of a meat meal versus fasting catabolism are the balance of amino acids (collagen aminos IN ADDITION TO muscle meat aminos), and calcium from the bones. Carbohydrates and sodium from the meal would also help signal to the body that a meal was eaten, since carbs and sodium are not speedily broken down by any tissues during fasting.
In summary, calcium, glycine (collagen), carbs, and sodium help the body distinguish between having just eaten a meal with nutrients to help rebuild the body (the ‘GO’ signal) versus a time of fasting with an out-pour of muscle meat aminos, phosphorus, and potassium.
Based on this approach, the following ratios are important to help promote a ‘growth’ metabolism:
Calcium : Phosphorus
Carbs : Protein (generally)
Glycine (Collagen) : Muscle Meat
Sodium : Potassium
Looking through this lens, eating too much potassium in a meal without a proper balance of sodium could be slowing to the metabolism. This is where, I think, the ‘alkaline’ focus loses (and where vegans suffer). Of course, our bodies need potassium and phosphorus and protein. But having salt with your fruit and tubers, and calcium and collagen with your meats and proteins will help ‘tell’ the body a meal was just eaten, and now it is time to grow. Otherwise, the body may go on presuming its is still fasting and continue to increase the stress hormones.
That sounds fascinating, Dan. I’ll look forward to it! Off to bed myself.