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Homocysteine Levels: Normal Range vs Optimal

Cardiovascular · Methylation

Your Doctor Called It Normal at 13. Here's Why I Wouldn't.

Homocysteine is one of the few markers on a standard panel where "in range" and "where you want to be" are two very different numbers — and where the gap has a measurable effect on the pressure inside your arteries.

By Dr. Andreas Boettcher, B.S., D.C., C.F.M.P. Board-Certified Chiropractic Physician · Certified Functional Medicine Practitioner · 33+ Years in Clinical Practice Ironman Triathlete · Master's Men's Physique Competitor

A man sat across from me last spring with two blood pressure medications in his file and a systolic reading that would not come below 145. He was fifty-two, not overweight, walked four miles most days, and had been told by three different providers that his labs were unremarkable.

I asked to see the panel. Everything flagged clean. Lipids acceptable, A1c 5.4, kidney function fine. And near the bottom, unflagged and uncircled, sat a homocysteine of 13.4 µmol/L. His lab's reference range topped out at 15, so the computer printed it in black rather than red and nobody said a word. That number had been in his chart for four years.

This is the error I want to talk about. Not a missed diagnosis — homocysteine is not a diagnosis. A missed signal. And because the internet is loud in both directions on this marker, I am going to walk you through what the evidence actually supports, including the parts that cut against the case I am making.

What homocysteine actually is

Homocysteine is not a toxin your body produces by mistake. It is an intersection.

Every time you eat protein you take in methionine. Your body converts methionine into S-adenosylmethionine, or SAMe — the universal methyl donor, the molecule your cells reach for whenever they need to attach a methyl group to something. They need to do that constantly: switching genes on and off, building neurotransmitters, making creatine, constructing cell membranes, clearing hormones.

When SAMe hands off its methyl group it becomes S-adenosylhomocysteine, which is broken down to homocysteine. So homocysteine is what is left over after your body spends a methyl group — metabolic exhaust from a process you want running hard.

The question is never whether you make homocysteine. You do, all day. The question is whether you clear it. There are exactly three ways out.

Figure 1 · The three exits

Homocysteine has three ways out, and each one needs different raw material

Exit 01 · Remethylation

The folate route

Enzyme: methionine synthase (MTR) · Requires: 5-MTHF + vitamin B12

The main road in most tissues. Methylfolate supplies a methyl group, B12 carries it across, and homocysteine becomes methionine again. This is the lane the MTHFR enzyme feeds — and the lane a common genetic variant constrains.

Exit 02 · Remethylation

The betaine route

Enzyme: betaine-homocysteine methyltransferase (BHMT) · Requires: betaine (TMG)

The parallel road, concentrated in liver and kidney. Betaine donates a methyl group directly. No folate required. No B12 required. This is the lane that keeps working when the folate lane is backed up — and it is the one almost nobody supplies deliberately.

Exit 03 · Transsulfuration

The one-way route

Enzymes: CBS, then CTH · Requires: vitamin B6 as P5P

The exit with no return. Homocysteine is committed downstream toward cysteine, and cysteine is the rate-limiting input for glutathione. Both enzymes in this lane depend on B6, which is why B6 status matters here as much as folate does upstream.

Read it as traffic, not chemistry. Homocysteine rises when arrivals outpace departures — which happens when the raw material for one or more exits runs short, or when the enzymes running them are constrained.

Two things follow. A high homocysteine is rarely a homocysteine problem — it is a report on the state of your methylation machinery. And the folate lane and the betaine lane are genuinely independent, so a person can be well supplied on folate and still have a bottleneck.

Where the MTHFR variant fits

Folate has to be converted into 5-methyltetrahydrofolate before it can do anything in Exit 01, and the enzyme running the last step of that conversion is MTHFR. A common variant, C677T, reduces its activity — two copies leaves it at roughly 30 percent of normal, one copy at roughly 65 percent. That is not a disease. It is a manufacturing constraint, and a common one.

Note what it means structurally: it narrows Exit 01 specifically. Exit 02 does not care about your MTHFR genotype at all. That is the single most useful thing to understand here, and we will come back to it. Worth adding, because it is almost always left out — riboflavin is the cofactor for the MTHFR enzyme itself, and riboflavin status measurably influences how well it performs, most notably in C677T carriers. A folate conversation that ignores B2 is missing an upstream lever.

How elevated homocysteine raises pressure inside the vessel

Here is the mechanism that connects this marker to the blood pressure cuff, and it runs through nitric oxide.

Nitric oxide is the molecule your endothelium — the single-cell lining of every vessel you own — releases to tell the vessel wall to relax. Less nitric oxide means less relaxation, which means a narrower tube, and pressure in a closed system is governed substantially by the diameter of the pipe.

Now follow the chemistry. Your cells produce ADMA (asymmetric dimethylarginine) as a normal byproduct of methylating arginine residues in proteins. ADMA resembles arginine closely enough to competitively block nitric oxide synthase, the enzyme that makes nitric oxide. Normally that is fine, because an enzyme called DDAH clears ADMA continuously.

Homocysteine interferes with DDAH. In work published in Circulation in 2001, Stühlinger and colleagues exposed endothelial cells to homocysteine and watched ADMA accumulate in a dose- and time-dependent way, alongside reduced DDAH activity and reduced nitric oxide production — an effect that held in cell-free systems, pointing to direct interaction with the enzyme.2

Plain language: homocysteine jams the disposal system for the molecule that blocks your vasodilator. The brake pedal sticks down. Not because anything is broken, but because the cleanup crew has been interfered with.

Corrosion, not laceration

The second mechanism is chemical, and the right mental picture is rust rather than injury.

A fraction of circulating homocysteine converts to homocysteine thiolactone, a highly reactive ring form produced when an enzyme called methionyl-tRNA synthetase makes an editing error. Thiolactone attacks the lysine residues on proteins and forms a permanent bond — a process called N-homocysteinylation. The protein it modifies changes shape, loses function, and becomes more vulnerable to oxidation. Jakubowski and colleagues demonstrated human endothelial cells doing exactly this conversion, in proportion to how much homocysteine was present.21

So the damage is not something scraping the vessel. It is a reactive compound corroding the machinery inside it, one protein at a time, at a rate set by how much substrate is circulating. That distinction is not academic. You cannot filter out corrosion. You can lower a substrate — which is the entire premise of the rest of this article.

There is a third, slower mechanism worth knowing. Elevated homocysteine has been associated with activation of matrix metalloproteinases, which degrade elastin and shift the arterial wall's elastin-to-collagen ratio toward stiffer collagen. This is where the pressure argument gets its teeth. A vessel that can no longer recoil the way it did at thirty stops absorbing each heartbeat and starts transmitting it — the same stroke volume against a less compliant tube produces a sharper pressure wave. Clinically that reads as rising systolic pressure and widening pulse pressure, which is the specific pattern most men over forty actually develop — and elevated homocysteine has been independently associated with isolated systolic hypertension in older adults.27 In a community sample of 1,680 adults, homocysteine was independently correlated with carotid-femoral pulse wave velocity, the standard measure of arterial stiffness — but only in the hypertensive subjects.3 I will come back to that "only," because it matters more than it looks.

Figure 2 · The signature chart

Two rulers, one number: what your lab calls normal versus where the risk data actually turns

Ruler 1 · What the lab report says

Normal — not flagged
Flagged

Ruler 2 · What the risk literature says

Target
Watch
Act
Work up
4 8 11 13 15 20

µmol/L · fasting plasma total homocysteine

A 13.4 sits in the middle of "normal" on the first ruler and in the middle of "act" on the second. Same number. Same patient. Two entirely different conversations.

The 15 µmol/L cutoff most labs use was derived to detect frank hyperhomocysteinemia, not to mark where cardiovascular and cognitive risk begins climbing. Observational risk rises continuously rather than switching on at a threshold, and the B-vitamin trials that showed brain-atrophy benefit selected participants above roughly 11 to 13 µmol/L.15,16 The ≤8 target is a functional-medicine convention built on that continuous gradient — it is a reasonable place to aim, not a validated trial endpoint. I am labeling it as the judgment call it is.
A reference range tells you where most people fall. It does not tell you where you want to be. Those are different questions, and only one of them is about you.

The honest complication

If I stopped here, I would be doing what most of the internet does with this marker, and you would eventually find out I had left something out. So let me hand you the strongest argument against my own position.

The large homocysteine-lowering trials mostly failed.

Through the 2000s researchers ran a series of major randomized trials giving B vitamins to lower homocysteine and looking for fewer heart attacks and strokes. NORVIT, in 3,749 post-heart-attack patients, found no benefit.9 VISP found no reduction in recurrent stroke.10 SEARCH found no effect on major vascular events.11 A 2010 meta-analysis pooling eight trials and 37,485 participants found that lowering homocysteine roughly 25 percent over a median five years produced no significant reduction in major vascular events.12

The observational data is more modest than it is usually presented, too. The Homocysteine Studies Collaboration — 30 studies, 5,073 coronary events — found that after adjustment, a 25 percent lower homocysteine (about 3 µmol/L) was associated with an 11 percent lower coronary risk and a 19 percent lower stroke risk. The authors' own conclusion: homocysteine is at most a modest independent predictor.1 The genetic evidence agrees. A meta-analysis of 75 MTHFR studies found the TT genotype carried an odds ratio of 1.16 for ischemic heart disease against CC, for a homocysteine difference of only 1.9 µmol/L.13,14

What I think that actually means

Not that the marker is worthless. Three things, stated carefully.

  1. Stroke and heart attack are not the same disease. HOPE-2 found a 25 percent reduction in stroke with B vitamins while finding nothing for myocardial infarction, and the authors treated the stroke result as a chance finding.8 That reading has been challenged since, because most heart attacks are plaque ruptures and many strokes are not. The pooled stroke data is consistently more favorable than the coronary data.
  2. Folate status changes everything. The strongest positive trial is CSPPT: 20,702 hypertensive Chinese adults randomized to enalapril alone or enalapril plus 0.8 mg folic acid. Over a median 4.5 years, first stroke fell from 3.4 percent to 2.7 percent — hazard ratio 0.79 — with the benefit concentrated in those with the lowest baseline folate.7 China does not fortify grain with folic acid. The United States has since 1998. That difference is probably why the American trials looked flat, and it is a real limit on how much CSPPT should move you if you eat a fortified Western diet.
  3. Causality likely runs both directions. Recall that the stiffness finding held only in hypertensive subjects. The authors' read was that homocysteine may not be a direct cause so much as a contributor to damage after vascular dysfunction has already begun.3 That fits what I see clinically. Insulin resistance, inflammation, poor kidney function and a nutrient-poor diet all raise homocysteine and all independently damage vessels.

So where does that leave blood pressure?

Somewhere more interesting than either camp will tell you.

I would not write that homocysteine is the cause of high blood pressure. That implies a primary causal role the outcome trials do not support. But lowering it is not inert either, and this is the part the skeptics skip.

Pooling 22 randomized trials across 41,633 participants, folic acid supplementation lowered systolic pressure by about 1.1 mmHg.22 Narrowed to hypertensive patients on high-dose folate, eight trials found systolic pressure down about 2 mmHg — and, more to the point of this article, flow-mediated dilation improved by 1.61 percent.23 That is the mechanism in this article showing up on an instrument. Not a marker moving. Actual vessel behavior.

Considerably larger effects have been reported in patients who have both hypertension and elevated homocysteine — one pooled analysis of 65 trials reported systolic down nearly 8 mmHg.24 I am not going to lean on that number. An effect that large sitting next to a 1.1 mmHg estimate drawn from six times as many participants is the classic signature of small-study and publication bias, and most of those trials were small and unblinded. I mention it because you will find it, and I would rather you hear the caveat from me.

One to two millimeters of mercury is not a treatment for hypertension and I will not dress it up as one. But it is a reproducible movement in the right direction from a nutrient, alongside a measurable improvement in endothelial function. That is a fair place to land: contributor, not sole cause. Elevated homocysteine is a reliable, cheap, actionable readout of methylation capacity, it travels with endothelial dysfunction and arterial stiffness, and it is one of the few numbers on a standard panel you can move with groceries and a capsule rather than a prescription.

What to ask your physician for

The workup that makes the number interpretable

A homocysteine value alone tells you there is traffic. It does not tell you which exit is blocked. Ask for these together:

  • Fasting plasma total homocysteine. Fast 8–12 hours; a protein-heavy meal can raise it meaningfully within hours.
  • Serum B12 and methylmalonic acid. MMA is the better functional marker — serum B12 can read normal while tissue status is not.
  • Red blood cell folate rather than serum folate, which reflects recent intake more than status.
  • Comprehensive metabolic panel with eGFR. Reduced kidney clearance is a leading and frequently missed cause of elevated homocysteine.
  • TSH with free T4. Hypothyroidism raises homocysteine and is easy to overlook.
  • A medication review. Metformin, proton pump inhibitors, methotrexate, several antiepileptics, and nitrous oxide exposure all affect B12 or folate status.17,18 None of these are bad drugs. They are context.
  • MTHFR genotyping — optional, and second. Genotype tells you about capacity. Homocysteine, B12 and folate tell you about status. Status first.

Retest 90 days after any change. A single value is a data point; two values are a direction.

The free levers, before anything else

These cost nothing and several of them move the number more than a capsule will. Do these first — not as a hurdle to clear before you're allowed to buy something, but because they address why the number is elevated in the first place.

  1. Eat the leafy greens, raw or barely cooked. Spinach, beets and wheat bran are among the densest natural sources of both folate and betaine, and betaine content drops significantly with cooking.19 Two cups of raw spinach and a beet is not a supplement strategy. It is groceries.
  2. Stop smoking. A well-established independent determinant of higher homocysteine, and it damages the endothelium through mechanisms that have nothing to do with methylation.17 Nothing on this page competes with this one.
  3. Look honestly at coffee volume. Heavy coffee consumption is a consistent determinant of higher homocysteine.17 I am not telling you to quit. I am telling you that if you are running six cups and a 14 µmol/L, those two facts know each other.
  4. Look honestly at alcohol. It interferes with folate absorption and B-vitamin status directly. I do not drink, and this is one of several reasons.
  5. Train. Physical activity is associated with lower homocysteine — and separately, blood flow across the vessel wall is the strongest natural stimulus for your own nitric oxide production. Exercise works both ends of this mechanism at once.
  6. Protect kidney function. Blood pressure control, glucose control, adequate hydration. If eGFR is drifting, that sits upstream of everything here.
  7. Reconsider antiseptic mouthwash. Small thing, real leverage: the dietary nitrate route to nitric oxide depends on oral bacteria to convert nitrate to nitrite, and antiseptic mouthwash disrupts exactly those bacteria. Raise it with your dentist rather than deciding alone.

A reader who does those seven things and never buys anything from me has done the majority of the available work. I want that on the record before the next section.

Know the number first

Do not supplement a marker you have not measured

Homocysteine is inexpensive to test and interpretable only alongside B12, folate and kidney function. If you want your labs read in context and a protocol built from your actual numbers rather than a guess, that is what the lab-based protocol is for.

Work With Dr. Andreas Lab-based protocols · See how it works

Where targeted support earns its place

Now the supplementation, and I want to be precise about what the evidence supports, because this is where the category gets loud.

Betaine, and the number that gets misquoted

Betaine — trimethylglycine, TMG, the same molecule — is the methyl donor for Exit 02. It has been used clinically since the 1980s for inherited disorders of homocysteine metabolism,20 and it works in ordinary people too.

You will see it claimed that 3 grams of TMG lowers homocysteine by up to 40 percent. That figure is being misapplied. In the randomized work from the Wageningen group, betaine lowered fasting plasma homocysteine by roughly 12 to 20 percent; the 20 to 40 percent figure describes reduction in post-methionine-load homocysteine — a provocation test, not your fasting lab value.5 Two different measurements, and the more dramatic one gets quoted for the more common situation.

The defensible numbers: in mildly hyperhomocysteinemic adults, 6 g/day lowered fasting homocysteine about 11 percent over six weeks, against 18 percent for 800 mcg of folic acid, with no significant difference between them.4 Doses within ordinary dietary range — 1.5 and 3 g/day — also lowered it measurably.5,6 A 2022 randomized crossover trial at 2.5 and 5 g/day moved homocysteine from 17.1 to 15.6 µmol/L over 21 days.21 Modest, consistent, real. That is the honest shape of the effect.

Figure 3 · Reading the label honestly

Which exits TMG Tri-Methyl Complex actually covers, and at what strength

Exit Per capsule Where the research sits Honest read
01 · Folate route
Folate, two forms		 2,000 mcg
3,400 DFE		 400–1,000 mcg
typical trials		 At trial strength. 1,000 mcg L-5-MTHF plus 1,000 mcg folinic acid. CSPPT moved first stroke in 20,702 people on 800 mcg of folic acid; this is more, in better forms.
01 · Folate route
Vitamin B12, two forms		 1,500 mcg 500–1,000 mcg
oral maintenance		 At therapeutic strength. 1,000 mcg methylcobalamin for the methylation enzyme, 500 mcg adenosylcobalamin for the mitochondrial one.
Upstream
Riboflavin, incl. R5P		 25 mg 1.3 mg
adult requirement		 Deliberate. Riboflavin is the cofactor for the MTHFR enzyme itself. Almost nobody puts it in a methylation formula on purpose.
03 · Transsulfuration
Vitamin B6		 50 mg 1.3–1.7 mg
adult requirement		 Generous. Both enzymes in this lane are B6-dependent. See the safety note below on long-term high-dose B6.
02 · Betaine route
Betaine anhydrous (TMG)		 400 mg 1,500–6,000 mg
betaine trials		 Supported, not saturated. Four times what our Methylated B carries, and still below the lowest dose that moved homocysteine on its own. It supplies the lane. It is not a standalone betaine dose, and I am not going to call it one.
Note what the name does not tell you. Despite "TMG" on the front, the heavy lifting in this formula is the folate and B12 — and that is the lane with the strongest human evidence behind it. The betaine is real support for the parallel route rather than a gram-level dose. If gram-level betaine is specifically what your labs call for, that is a conversation about a different product, and you should hear that from me rather than discover it later.

So the pairing has a structure, and the two pieces do genuinely different jobs.

TMG Tri-Methyl Complex works the clearance side. One capsule supplies all three exits from Figure 1 — folate and B12 at trial strength for Exit 01, betaine for Exit 02, B6 for Exit 03, plus the riboflavin that MTHFR itself runs on. That last detail matters more than it sounds. If your folate lane is narrowed by a C677T variant, giving you 1,000 mcg of already-methylated folate skips the constrained step entirely, and the betaine lane runs regardless of your genotype.

Nitric Supreme works the output side. If elevated homocysteine suppresses nitric oxide by jamming DDAH, then clearing homocysteine addresses the interference — and supporting nitric oxide production addresses what the vessel actually does about it. It covers both routes to nitric oxide: dietary nitrate from 1,500 mg of organic beets, and the enzymatic route via 1,500 mg of Nitrosigine® plus citrulline malate. It also carries a polyphenol and antioxidant matrix, which is not decoration — nitric oxide has a half-life measured in seconds and is consumed by exactly the oxidative stress this article has been describing.

Two products, two ends of one mechanism: stop the corrosion, support the dilation.

Before you stack anything

These two overlap on purpose. Do not add a third.

Nitric Supreme carries its own methylation support — 680 mcg DFE of L-5-MTHF, 200 mcg of B12 across two forms, 7.25 mg of P5P and 200 mg of betaine from beet root extract. Run it alongside TMG Tri-Methyl Complex and those amounts add. That is intentional and the combined totals remain sensible, but you should know it rather than discover it.

What I would not do is add a third methylation product on top. Our Methylated B and Daily Multi both carry folate, B12 and B6 as well, and B6 in particular is worth adding up across every bottle on your counter — sustained high intakes are associated with peripheral sensory neuropathy. Pick a lane. If you take this pairing, that is your methylation coverage handled.

Bring every label to your physician or pharmacist, and if you develop new tingling or numbness in your hands or feet, stop and get seen promptly.

Honest expectations

What betaine will not do, and one caveat you deserve up front

It will not lower your blood pressure. This is a dietary supplement supporting normal homocysteine metabolism. It is not a treatment for hypertension and it is not a substitute for prescribed medication. Never stop or adjust a blood pressure medication on your own.

It is not a substitute for fixing why the number is high. If your homocysteine is elevated because your kidney function is declining, or because a medication is depleting your B12, no methyl donor addresses that. It works around the traffic. Clearing it is a different job, and it belongs to you and your physician.

The lipid question, in proportion. You may run into this, so here it is. In pooled randomized data, 6 grams a day of standalone betaine raised LDL cholesterol about 11 percent and triglycerides about 13 percent.25 That finding is real and worth knowing — and it is fifteen times the 400 mg in this formula. Doses of 1.5 and 3 grams did not reach significance, and a 2022 trial at 2.5 and 5 grams found no lipid effect at all.26 The proposed mechanism is increased export of fat out of the liver as VLDL, which is also why betaine is studied in fatty liver disease. Lipid leaving the liver and lipid accumulating in an artery are not the same event, and those trials were not built to tell them apart.

My read: this is a high-dose, standalone-betaine phenomenon that does not apply at the amount in this product. I am telling you anyway, because a reader who finds it later and thinks I hid it has every right to distrust the rest of this page. Retest a lipid panel alongside your homocysteine at 90 days regardless — you should be watching both numbers anyway.

Exit 02 · The lane MTHFR cannot narrow

TMG Tri-Methyl Complex

Trimethylglycine supplies the betaine remethylation route directly — no folate required, no B12 required, no dependence on the enzyme a common variant constrains. Supports normal homocysteine metabolism and normal methyl-group availability.

View TMG Tri-Methyl Complex Pairs with Nitric Supreme for the nitric oxide side

Back to the man with the 13.4

He did not have a homocysteine disease. He had a number nobody had ever explained to him, sitting quietly inside a reference range built for a different question.

What he got was a real workup — B12 with methylmalonic acid, red cell folate, kidney function, thyroid, and a medication review that turned up a long-standing proton pump inhibitor. What he changed cost him nothing: more greens, less coffee, and a conversation with his physician he had not known to ask for. What he added was targeted and chosen after the labs rather than before.

I am not going to tell you his blood pressure normalized, because one man's outcome proves nothing and I do not build articles on anecdotes. What I will tell you is that he stopped being a man with an unexplained number and became a man with a direction — and that his physician finally had something to work with besides a third prescription.

That is the whole argument. Not that homocysteine is the hidden cause of everything. That it is a cheap, measurable, movable readout of how well your methylation machinery is running, and that "not flagged" and "where you want it" are two different standards — only one of which was ever about you. You played the first half against a reference range designed to catch disease. The second half is where you get to play for optimal instead, and that is the half that decides the outcome.

Build the foundation, then accelerate it

Support both ends of the same pathway

Clear the interference and support the output. TMG Tri-Methyl Complex for the betaine remethylation lane, Nitric Supreme for nitric oxide production and vascular support. Train, eat the greens, fix the sleep, get the workup — then use targeted support to accelerate what the foundation started.

Shop TMG Tri-Methyl Complex Pairs with Nitric Supreme · Lab-based protocols

Stay Strong,

Dr. Andreas Boettcher, B.S., D.C., C.F.M.P.

Ironman Triathlete · Master's Men's Physique Competitor

Medical Disclaimer

This article is provided for educational purposes only and does not constitute medical advice, diagnosis or treatment for any individual. Elevated homocysteine, elevated blood pressure, and the symptoms discussed here may reflect serious underlying conditions — including kidney disease, thyroid disease, vitamin B12 deficiency, cardiovascular disease and inherited metabolic disorders — that warrant evaluation by a qualified physician. Do not start, stop, or change the dose of any medication or dietary supplement on the basis of this article.

Consult your physician or pharmacist before supplementing, particularly if you are pregnant, nursing, or taking antihypertensive medications, nitrates, PDE5 inhibitors, anticoagulants or antiplatelet drugs, methotrexate or other folate antagonists, antiepileptic drugs, metformin, proton pump inhibitors, or levodopa. Betaine supplementation has been shown to raise LDL cholesterol and triglycerides at higher doses; if you are managing elevated lipids, discuss this with your physician before beginning and monitor a lipid panel. Uncontrolled hypertension is dangerous and largely symptomless — never reduce or discontinue a prescribed blood pressure medication without your physician's direction.

FDA Statement

These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease.

Trademark Attribution

Nitrosigine is a registered trademark of Nutrition 21, LLC. Magnafolate is a registered trademark of Lianyungang Jinkang Pharmaceutical Technology Co., Ltd. All other trademarks are the property of their respective owners. IOH Nutrition LLC is not affiliated with, endorsed by, or sponsored by these trademark holders.

Manufacturing

IOH Nutrition products are manufactured in the United States in FDA-registered, cGMP-compliant facilities. FDA registers manufacturing facilities; it does not approve them or the dietary supplements produced in them.

References

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  5. Olthof MR, van Vliet T, Boelsma E, Verhoef P. Low dose betaine supplementation leads to immediate and long term lowering of plasma homocysteine in healthy men and women. J Nutr. 2003;133(12):4135–4138.
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