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Reply To: Fructose Malabsorption

Blog Forums Nutrition Fructose Malabsorption Reply To: Fructose Malabsorption


Hey Dan,

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.’threads/why-is-potassium-supplementation-needed-in-methylation-treatmt.18670/

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.

Humbly, CP