Nutricura Diëtistenpraktijk

17/02/2026

Glycine works for sleep but doesn't work like a typical "sleep supplement." It works like a thermostat.

When you take 3g of glycine before bed, it crosses the blood-brain barrier and binds to NMDA receptors in the suprachiasmatic nucleus, the brain's master circadian clock. This activates the medial preoptic area, which triggers peripheral vasodilation: blood flow increases to your hands and feet, heat radiates out through the skin, and your core body temperature drops. That temperature drop is the same signal your body produces naturally before sleep onset. Glycine just makes it happen more reliably.

This was mapped at Stanford by Kawai and colleagues. When they ablated the SCN in animal models, glycine's sleep-promoting and hypothermic effects disappeared entirely, confirming this is the target, not a downstream side effect. In human trials, 3g before bed reduced sleep-onset latency and next-day fatigue in volunteers with sleep complaints.

Polysomnographic data showed improved subjective sleep quality correlated with the temperature shift. The practical detail nobody mentions: glycine is one of the cheapest amino acids on the market. A 3g dose costs roughly nine cents. It has no sedative hangover because it isn't a sedative. It works through the same thermoregulatory cascade that a hot bath before bed exploits, peripheral vasodilation leading to core cooling, except it initiates it centrally rather than peripherally.

*None of this means glycine replaces sleep hygiene or addresses underlying sleep disorders. .

Kawai et al., Neuropsychopharmacology, 2015
Bannai et al., Frontiers in Neurology, 2012
Yamadera et al., Sleep and Biological Rhythms, 2007

17/02/2026

Homocysteine is a sulfur-containing amino acid produced during normal methionine metabolism, but when it accumulates it becomes strongly pro-oxidative and damaging to vascular tissue. Elevated homocysteine has been linked to endothelial dysfunction, cardiovascular disease, pregnancy complications, and accelerated cellular aging. While homocysteine is often framed as a folate or MTHFR problem, the biochemical reality is that homocysteine toxicity is driven largely by oxidative stress, making antioxidant capacity one of the most critical and overlooked regulators of homocysteine levels.

Vitamin C(ascorbic acid is the purest form) plays a central role in this regulation. Multiple human studies demonstrate an inverse relationship between plasma vitamin C levels and circulating homocysteine. One large analysis concluded that “vitamin C levels showed an inverse correlation with homocysteine levels,” meaning higher vitamin C status was consistently associated with lower homocysteine concentrations . This relationship held even when controlling for folate and B vitamin status, suggesting vitamin C exerts an independent effect on homocysteine metabolism rather than acting solely as a supporting nutrient.

The mechanism is rooted in redox biology. Homocysteine exerts much of its harm by generating reactive oxygen species that impair endothelial nitric oxide signaling and damage vascular walls. Vitamin C directly neutralizes this oxidative stress. In a controlled human study examining endothelial dysfunction induced by elevated homocysteine, researchers found that “an elevation in homocysteine-induced oxidative stress and endothelial dysfunction can be prevented by pretreatment with vitamin C in healthy subjects” . This finding is critical because it shows vitamin C does not merely lower homocysteine on paper, but actively protects tissues from its downstream damage.

Beyond protection, vitamin C also appears to influence homocysteine clearance. A review published in Antioxidants reported that ascorbic acid supplementation “may decrease serum levels of homocysteine, which is considered a biomarker of cardiovascular disease risk” . This suggests vitamin C supports the biochemical systems responsible for recycling or neutralizing homocysteine, particularly under conditions of oxidative stress, inflammation, or increased metabolic demand such as pregnancy.

Population studies reinforce these findings. In hypertensive and aging populations, higher dietary vitamin C intake was associated with a significantly lower risk of elevated homocysteine. One large cohort analysis described a clear linear inverse relationship between vitamin C intake and hyperhomocysteinemia, indicating that as vitamin C intake increased, homocysteine levels decreased in a dose-responsive manner . This relationship held across genetic backgrounds, underscoring that vitamin C’s role is not limited to individuals with known MTHFR variants.

Vitamin C also reduces reliance on folate-dependent pathways by stabilizing redox balance. When oxidative stress is high, homocysteine recycling through methylation becomes inefficient regardless of folate intake. By lowering oxidative burden, vitamin C restores enzymatic efficiency and reduces the need for aggressive methyl donor supplementation. This explains why many individuals see homocysteine normalize with adequate vitamin C alone, even when folate intake is modest or minimal.

The literature makes a compelling case that vitamin C is not a peripheral nutrient in homocysteine regulation but a primary one. It lowers oxidative stress, protects vascular tissue, supports enzymatic recycling of homocysteine, and reduces dependence on genetically fragile methylation pathways. Homocysteine is not simply a gene issue. It is a redox issue, and vitamin C sits at the center of that control system. Follow us for more!

17/02/2026

https://www.youtube.com/watch?v=dFc_5sBj5eY

After 7 years of prescribing and monitoring high-dose vitamin D therapy (60,000 IU daily), we are releasing our real clinical observations. This video explor...

29/01/2026

Zucht.

Er wordt gewaarschuwd voor de gevolgen, onder meer voor de consumptie door kinderen. ➡ https://tinyurl.com/wwdwfusd

28/01/2026

Op 81-jarige leeftijd doen de meeste mensen het wat meestal rustiger aan, behalve deze Spaanse man. Hij verbrak echter het wereldrecord op de 50 km in zijn leeftijdsgroep… en liep sneller dan de meeste 30-jarigen. Onderzoekers publiceerden onlangs zijn statistieken:

Leeftijd: 81. VO₂ max (hardlopen): 52,8 mL/kg/min.
De hoogste ooit gemeten bij iemand van 80+.
Vergelijkbaar met ongeveer het 70e percentiel van mannen van 20–30 jaar. Hij verbrak ook het marathon- en 50 km-wereldrecord in zijn leeftijdsgroep. Hij begon pas met hardlopen op zijn 66e en ging pas wedstrijden lopen in zijn 70er jaren. Hierbij een video over deze man, hij is waarschijnlijk de fitste 81-jarige ter wereld: https://youtu.be/OVBd9QgLFQQ

VO₂ max is één van de sterkste voorspellers van overleving.
Je bent tot veel meer in staat dan je denkt, zelfs op latere leeftijd.

Cardiorespiratoire fitheid (VO₂ max) is sterk verbonden met sterfte door alle oorzaken. In veel studies een betere voorspeller dan voedingskwaliteit. Het verschil tussen zelfstandig blijven in je 70- en 80-er jaren… of niet.

Je hoeft geen wereldrecordhouder te zijn, maar je wilt wél dat je VO₂ max, kracht en dagelijkse beweging omhoog blijven gaan, niet omlaag.

Naast de VO₂ max-resultaten ervoeren deelnemers ook het volgende.

Join our LONGEVITY and ANTI-AGING Skool Community: https://www.skool.com/youthspan-society-9710/My 2026 longevity routine: https://youtu.be/OceysodInIoFull g...

23/01/2026

Most of the world isn’t getting enough omega-3, and the problem isn’t optimization. It’s the floor.

A global review of national and international nutrition guidelines shows that ~76% of people worldwide fail to meet the recommended intake of omega-3 fatty acids EPA and DHA. This gap isn’t subtle, it represents one of the most widespread nutrient shortfalls affecting otherwise healthy populations.

What’s often misunderstood is what the recommendation actually represents.

The most frequently cited target (~250 mg per day of combined EPA + DHA) is not a “maximum benefit” dose.
It is the minimum intake consistently associated with measurable health protection, particularly a reduced risk of fatal coronary heart disease and sudden cardiac death.

Large population datasets show that cardiovascular risk declines as EPA+DHA intake increases, but this decline plateaus around 250 mg/day. Below that level, risk rises. Above it, additional benefits may occur, but the core mortality signal is already established.

That is why organizations such as FAO/WHO, EFSA, and numerous national health authorities converge on this number.

In other words:
This guideline defines the bare minimum needed to experience benefit, not an optimal or therapeutic dose.

Yet most people aren’t even reaching that baseline.

Food-based strategies alone often fall short due to:

Low oily fish consumption

Cultural and geographic barriers

Sustainability concerns

Confusing and inconsistent guidelines between countries

As a result, the review highlights that supplementation or enriched foods are often required, particularly during pregnancy and in individuals with low fish intake.

Pregnancy recommendations build on the same baseline, typically advising 250 mg EPA+DHA plus an additional 100–200 mg DHA, reflecting increased biological demand, not a different philosophy.

Omega-3s support health across the entire life course, from fetal neurodevelopment and visual function to cardiovascular health, immune regulation, and healthy aging. But none of those benefits matter if people never reach the threshold where benefit begins.

This isn’t about doing everything possible.
It’s about doing enough to matter.

20/01/2026

COPPER DEFICIENCY MAY BE A LEADING CAUSE OF HEART DISEASE

If you watched the Olympics in 2016, then you may remember the commercial that said we all have a little bit of gold inside of us (0.02 mg to be exact); with most of that gold being contained in our heart, "There's (Literally) a Little Gold in Everyone".

But there’s a more precious metal when it comes to this vital organ...and that metal is copper.

When we think of copper we normally think of a penny, cookware, or perhaps even jewelry, but copper is actually an essential trace metal that we need to consume in our diets or else we would perish (hence the word ‘essential’).

Another thing that you maybe didn’t know about copper, and your cardiologist probably doesn’t know either, is that a lack of copper in the diet produces almost every single risk factor for heart disease. Indeed, a lack of copper in the diet can lead to elevated blood glucose, lipids (total and LDL cholesterol), uric acid, blood pressure and abnormal electrocardiograms, which has been known since at least 1987.

Importantly, some of these changes have occurred even at intakes that are considered “adequate”. A lack of copper also increases the susceptibility of lipoproteins and tissues to oxidize, and oxidized lipids are now thought to be one of the biggest drivers of heart disease. In other words, if your diet is lacking in copper, the so-called “bad LDL-cholesterol” in your body is more likely to oxidize, leading to atherosclerotic plaque formation and heart disease.

That’s a scary thought!

But why does any of this matter? Surely most of us aren’t copper deficient or we would all know about it. Unfortunately, there is no easy way to diagnose copper deficiency since blood levels are inaccurate for measuring true copper deficiency. This is because inflammation increases copper levels in the blood (serum copper levels likely become elevated in the blood to help fight inflammation).

In other words, blood levels of copper only diagnose severe copper deficiency but miss subclinical copper deficiency and normal copper levels in the blood are essentially meaningless (hence the issue).

So, are we getting enough copper in our diet?

The most shocking fact about the copper-heart disease story is that the safe and adequate intake of copper (originally established in 1980) was set between 2 and 3 mg per day. However, it was discovered that very few people in the United States consumed this amount of copper and that posed a problem (i.e., necessitating copper supplementation to meet the adequate intake for almost everyone in the United States). That is likely why the adequate intake for copper was subsequently lowered to just 0.9 mg/day. And this was primarily based on one small study looking at just eleven healthy young men. However, other studies suggested that we needed at least 1.3 mg/day of copper to meet our requirements. And yet most Americans (and most people around the world) may not even be consuming this amount of copper each day.

So why is copper deficiency virtually unknown? Perhaps because we have been so focused on obesity (over-eating) that we have totally neglected the harms of under-eating (in this case, a lack of dietary copper).

Even if we did consume the “adequate intake” of copper each day (which is still a matter of debate), we are now living in a society that predisposes us to copper deficiency. As a colleague and I published in an previous New York Times Op-Ed, the average American now consumes over 100 pounds or more of the sweet stuff per year. Furthermore, overconsuming sugar leads to copper deficiency as it reduces the absorption of copper in the intestine.

Additionally, numerous disease states predispose to copper deficit, such as kidney disease, celiac disease and even bariatric surgery (with over 200,000 of these operations being performed in the United States alone each year). Zinc-containing denture creams also put the elderly at risk for copper deficiency. Any way you slice it, copper deficiency is likely an under-diagnosed problem.

So, what does the evidence in the literature say about copper supplementation? One study in 16 healthy young women supplemented the diet with 3-6 mg of copper per day and noted, “we found that the young female volunteers who participated in this study appeared to be marginally copper deficient when consuming their habitual diet.” https://pubmed.ncbi.nlm.nih.gov/16115357/

The authors also noted that supplementing with 6 mg of copper/day reduced a substance in the blood that inhibits the breakdown of blood clots. In other words, a lack of copper in the diet may predispose to more blood clots, whereas ensuring adequate copper intake may have the reverse effect.

Another study, this time in 60 patients with high blood pressure, found that 62% of study participants were marginally copper deficient and that supplementing these individuals with 5 mg/day of copper significantly reduced their blood pressure https://pubmed.ncbi.nlm.nih.gov/14694810/.

Another study in 73 patients with high lipid levels noted that 38% of the study participants were marginally copper deficient and found that supplementing with 5 mg of copper/day decreased total cholesterol, the bad (LDL)-cholesterol and triglycerides and increased the good (HDL) cholesterol. https://pubmed.ncbi.nlm.nih.gov/15969266/

In other words, if you take a group of individuals, around 1/3rd to 2/3rds have marginal copper deficiency and supplementing their diet with copper improves many health parameters.

Importantly, good dietary sources of copper (such as liver, oysters, lobster, crab and avocados) are not dietary staples for most Americans.

Moreover, eating a diet high in muscle meat without consuming organs increases the risk of copper deficiency as muscle meat contains a zinc to copper ratio of 50:1 (zinc inhibits the absorption of copper), whereas organ meats (liver for example) have a zinc to copper ratio of just 1.7:1.

Thus, our current dietary pattern is undoubtedly contributing to the problem of copper deficiency.

The optimal intake of copper per day for most people seems to be somewhere between 2.5 to 6 mg per day.

So, if we want to win the gold when it comes to our heart health; it may depend on a different metal...a metal all of us should have a greater appreciation for... copper!

How do I get copper?

1. I consume organ blends from NorthStar Bison https://northstarbison.com/collections/ground-beef-patties-100-grass-fed-and-finished/products/beef-old-world-ground-blend?rfsn=6160609.f40c9d. DRJAMES = 10% off.

2. A copper supplement https://t.co/GBVDCTadXP. Autofill saves 15% and my Fullscript accepts HSA/FSA.

If you want to learn about copper and 23 total minerals check out my book The Mineral Fix https://amzn.to/3aHoeu9

20/01/2026

VITAMIN D Does NOT Work WITHOUT MAGNESIUM and VITAMIN K2

If you’re taking vitamin D3 without magnesium and vitamin K2 you're not getting the full benefits and in some cases you could even be increasing risk.

Here’s how the system actually works:

1. Vitamin D3 — Calcium Absorption

Vitamin D3 helps your body absorb calcium from food and supplements.

Without enough D3, calcium absorption is poor.

2. Vitamin K2 — Calcium Direction

Vitamin K2 tells calcium where to go:

✔ Into bones and teeth

❌ Not into arteries or soft tissues

Without K2, absorbed calcium can accumulate in blood vessels, contributing to arterial calcification.

3. Magnesium — Vitamin D Activation

Magnesium is required to activate vitamin D.

It converts vitamin D into the active hormone 1,25-dihydroxycholecalciferol (calcitriol).

Around ~50% of people are magnesium deficient, which can silently block vitamin D from working.

Why This Matters

Taking vitamin D alone can:

- Increase calcium absorption without proper regulation (arterial calcifications)

- Stress magnesium stores

- Reduce the effectiveness of vitamin D over time

The Takeaway

Vitamin D + K2 + Magnesium = a functional system

Together, they support:

- Strong bones and teeth

- Healthy arteries

- Better sleep and stress resilience

- Proper calcium metabolism

- Overall metabolic and cardiovascular health

If you want to see the magnesium and Vitamin D3/K2 that I take create an account here https://us.fullscript.com/protocols/ddinicolantonio-general-health

17/01/2026

Hoe een lowcarb of keto ontbijt er kan uitzien. Zo simpel dus. Ook geen zin in een crash van je bloedsuikerspiegel enkele uren na je ontbijt? Probeer het dan zeker eens uit 🤪.

Ingrediënten:
- 3 eieren
- 1 sneetje prosciutto ham
- 50g parmigiano kaas
- 20 pecannoten
- 1 low cracker (bolletje)

16/01/2026

Interessant artikel uit de knack.

09/01/2026

Decennia lang werd ons verteld dat granen (brood, pasta, rijst, cereals) de basis moesten vormen van ons eten: 6-11 porties per dag volgens de klassieke Food Guide Pyramid uit 1992. veel koolhydraten onderaan, vetten en eiwitten bovenaan (en spaarzaam gebruiken).
Die aanpak is nu officieel op z'n kop gezet.

Waarom promootten wetenschappers & overheden decennia de "grain-heavy" piramide?
De oorsprong gaat terug naar de jaren 70-80, met sterke invloed van:
• Ancel Keys en zijn (later zwaar bekritiseerde) "lipid hypothesis" die verzadigd vet als hoofdschuldige van hartziekten zag.
• Lobby van graan-, suiker- en voedingsindustrie (denk aan Kellogg's, General Mills, etc.) die baat hadden bij een piramide met granen als basis.
• De suikerindustrie betaalde in de jaren 60 wetenschappers om de schuld naar vet te schuiven (dat kwam later uit via oude documenten).

👉 Resultaat? Obesitas, diabetes type 2 en metabole ziektes explodeerden sinds de jaren 90, terwijl de piramide juist het omgekeerde adviseerde van wat veel mensen nu als beter ervaren (meer proteïne + vet, minder geraffineerde carbs).

En nu in 2026?
De nieuwe richtlijnen draaien het om:
Focus op "real food": proteïne (vlees, vis, eieren), volle zuivel, gezonde vetten (avocado, olijfolie, noten, boter), veel groenten & fruit.
Whole grains zijn er nog steeds, maar veel kleiner (onderaan de piramide).
Sterke waarschuwing tegen ultra-processed foods, added sugars en geraffineerde koolhydraten.

Dus ja… de wetenschappers en beleidsmakers van toen? Die zijn nu behoorlijk stil, of ze proberen het nog te verdedigen met "toen wisten we niet beter". Maar de shift is er: van koolhydraat-dominant naar proteïne- & vet-rijk + volle producten.
Eindelijk gerechtigheid voor de biefstuk, eieren en volle yoghurt! 🥩🥚🧈

Wat vind jij?😏
Ga jij je eetpatroon nog verder aanpassen aan deze "nieuwe" piramide?

09/01/2026

Deze lekkere, eiwitrijke/vezelrijke crackers met minder koolhydraten zijn nu 1 + 1 gratis in de Albert Heijn! Allen daarheen zou ik zeggen 😁😁😁