Take Enough Vitamin D3

Many people supplement with 300 to 400 IU of vitamin D3, but do they take enough vitamin D3? There is a simple way of finding out: ask your doctor to order a 25-hydroxyvitamin D blood test.   This will show whether the gut absorbed enough of the essential vitamin. It will also show whether or not your vitamin D3 capsules or tablets were strong enough. It is now generally accepted that a good range of the vitamin D blood level is between 50 and 80 ng/ml. Unfortunately many Americans who come down with various diseases have blood levels of less than 30 ng/ml. Here are some facts about what a lack of vitamin D3 can cause.

Increased risk of mortality with lower vitamin D levels in ICU patients

  1. A New England Journal study from 2009 reported about 1100 patients in Intensive Care Units (ICU). Their average vitamin D blood level was only 16 ng/ml. They tracked the mortality rates depending on the vitamin D blood level. Insufficient vitamin D levels showed an association with a mortality rate of 45%. An intermediate level had a mortality rate of 35%. And a satisfactory level of vitamin D had a mortality of only16%. Between the low level of vitamin D and the normal level there was a 3-fold difference in mortality!
  2. Another study from 2015 repeated the mortality study with 135 ICU patients. Researchers correlated Vitamin D blood levels with mortality rates of patients. When vitamin D levels were below 12 ng/ml, there was a mortality rate of 32.2%. Patients with higher levels of vitamin D had a mortality rate of 13.2%. The authors concluded that vitamin D blood levels were an independent risk factor for mortality. Patients less than 12 ng/ml had a 2.4-fold higher risk of dying than patients with normal vitamin D levels.

Do patients with multiple sclerosis take enough vitamin D3?

Perhaps one of the earliest results of vitamin D3 research was the following observation. More than 90% of patients with multiple sclerosis were deficient in vitamin D blood levels. Their levels were below 20 ng/ml. Other researchers showed that vitamin D could directly tone down the aggressiveness of the immune cells of MS patients. These were the ones that attacked the myelin sheath. As a result of this knowledge it is important for MS patients to take high enough vitamin D3 supplements. When they reach good vitamin D blood levels their MS is better controlled.

Canada as a northern country has 291 MS patients per 100,000 people. Contrast this to 110-140 MS patients per 100,000 people in the northern US (between the 37th parallel and the US/Canadian border). In addition south of the 37th parallel there are only 57-78 cases of MS per 100,000 people. Researchers have concluded that the less sun light people get, the higher the rate of MS in the population will be. However, instead of sun exposure you can supplement with vitamin D3 capsules to get the blood vitamin D levels up to the range of between 50 and 80 ng/ml.

Do stroke patients take enough vitamin D3?

Strokes are very common. About 6.8 million Americans survive a stroke and live with various disabilities. 15% die shortly after their stroke. 40% are left with moderate to severe disabilities. Many require special care.

  1. Studies have shown that patients with the lowest level of vitamin D have the poorest functional outcomes. Moreover, for every 10 ng/ml decrease in vitamin D levels the odds of a healthy recovery 3 months after the stroke fell by about half. This was independent of age and the initial stroke severity.
  2. In another 2015 study from South Korea 818 stroke patients took tests to evaluate whether they had adequate vitamin D blood levels. There was a clear division between those whose levels were higher than 10 ng/ml or lower. When the vitamin D level was higher, there was a 90% better recovery from their stroke after 3 months. In comparison those whose vitamin D levels were below 10 ng/ml had poor recovery rates. Experts say that vitamin D levels should stay in the range between 50 and 80 ng/ml. This will prevent numerous diseases.

Do diabetics take enough vitamin D3?

  1. Vitamin D3 can silence diabetes genes in connection with the right diet and cofactors of zinc and magnesium. A Mediterranean diet can stabilize the metabolism and fight inflammation. Zinc and magnesium are important cofactors in enzymes necessary to prevent diabetes. Vitamin D3 and omega-3intake are helping to control inflammation and preserve beta cells in the pancreas in diabetes patients. This is important for continued production of insulin.
  2. A Chinese research team found that vitamin D3 protects beta cells in the pancreas from dying off. The finding was that vitamin D3 receptors in the insulin producing cells prevented the dying off of these cells, as long as there was enough vitamin D available. Insulin production by the pancreas remained effective. And insulin is vital for long-term survival of diabetes patients. The key for diabetes patients is to take adequate doses of vitamin D3 to protect their insulin producing beta cells.
  3. A 2015 Italian study showed that micro vascular complications in diabetes patients were high, if the vitamin D3 blood levels were low. If patients had high levels of vitamin D3, there were no complications such as retinopathy or nephropathy. But if levels were below 20 ng/ml, damages were significant in the capillaries of the eyes and kidneys.

Do patients with inflammatory conditions take enough vitamin D3?

What do the lining of the arteries, the inflamed joints, a degenerative meniscus and heart attacks and strokes have in common? It is the inflammation that changes the body chemistry. It gets even more complicated, because the extra calories that we consume get stored as visceral fat. This is done automatically when you eat too much sugar and starchy foods. When the glycogen stores are full, any surplus sugar gets metabolized by the liver into triglycerides, fatty acids and LDL cholesterol and gets stored as body fat. The most active fat is the visceral fat between our guts and around our body organs. This produces interleukins and other inflammatory cytokines that circulate in the blood causing inflammation in all our arteries. Interleukin-6 is an inflammatory cytokine. High interleukin-6 levels contribute to causation of various cancers.

This 2015 study from Seattle University followed 218 obese postmenopausal women with a body mass index of larger than 25.0 for 12 months. Both received weight loss intervention and either 2000 IU of vitamin D3 daily or a placebo pill. Both groups lost about 5 to 10% of weight in 12 months. However, the interleukin-6 level of the vitamin D3 group had a reduction of 37.3%. This was in stark contrast to the placebo group where the interleukin-6 level reduction was only 17.2%. This type of research shows the incredible power of vitamin D3. This likely is the reason why several cancer frequencies can show a reduction with regular vitamin D3 supplementation.

Attention deficit disorder and vitamin D3

  1. Other research compared a group of 37 children with attention deficit hyperactivity disorder (ADHD to 37 normal children. Blood levels of vitamin D were 19.11±10.10 ng/ml in the ADHD group and 28.67±13.76 ng/ml in the normal group. Other researchers have found similar findings, establishing that very low vitamin D levels have a connection with ADHD.
  2. A prospective study from Spain involving 1,650 mother-child pairs investigated the effect of mother’s vitamin D level during her pregnancy with the risk for ADHD by the time the child was 4 to 5 years old. Schoolteachers followed the standard test procedures to establish the ADHD diagnosis. The study showed that for every 10-ng/ml increment of the mother’s blood vitamin D level during her pregnancy the children had 11% less ADHD-like symptoms. The authors cautioned that it takes mega doses of vitamin D3 to reach these kinds of results. The usual 400 IU of vitamin D3 per day will not achieve the desired increase of vitamin D3 levels, but amounts of 5,000 IU to 8,000 IU are necessary to achieve this.

Schizophrenia and vitamin D3

A 2014 Meta analysis found that low vitamin D levels have an association with a 2.16-times higher probability of having schizophrenia than controls with normal vitamin D levels. Another study examined whether those patients who had an acute psychosis would have lower vitamin D blood levels than schizophrenia patients in remission or control patients without schizophrenia. Studies compared 40 patients with an acute psychosis to 41 patients in remission and 40 healthy controls. Patients with an acute psychosis had extremely low vitamin D blood levels, while patients in remission had much better vitamin D levels. Healthy controls had the best vitamin D levels.

Absorption and metabolism of vitamin D3

Magnesium plays a central role in activating vitamin D3. This publication points out that magnesium is also necessary for absorption of vitamin D3 in the gut. The activation of vitamin D3 is also partially responsible for vitamin D absorption. Both vitamin D3 and magnesium play an important role in bone and calcium metabolism. The fact that every body cell has vitamin D3 receptors shows how important it is for the maintenance of the body. Many researchers say that vitamin D3 qualifies as a hormone because of the specific effects on cells via vitamin D3 receptors.

Take Enough Vitamin D3

Take Enough Vitamin D3


Vitamin D3 is an important signaling hormone and vitamin that regulates the body’s calcium absorption and is responsible for bone metabolism. Research has shown that the lack of vitamin D3 causes several unrelated diseases, like rickets, multiple sclerosis, and schizophrenia. But other diseases, where a lack of vitamin D3 was present, were diabetes, attention deficit disorder and strokes. When patients with elevated inflammatory markers take vitamin D3 their interleukin-6 levels dropped by 37.3%. To achieve this, patients needed to consume at least 2000 IU. We all should have our vitamin D blood level measured from time to time. It should be between 50 and 80 ng/ml. Too many Americans are deficient in vitamin D3 and come down with the diseases mentioned! Prevention and supplementation go hand in hand. You can prevent a lot of diseases this way.



Melatonin More Than A Sleeping Aid

Melatonin has been available to the public in the US since 1992. It is usually used as a sleeping aid or for jet lag related sleeping problems. However, in the last decade much more data about melatonin has come out that has proven that melatonin is a major hormone. The pineal gland contains another brain hormone, serotonin, which is converted into melatonin within that gland. Melatonin is a key hormone that regulates the sleep/wake cycle. It works in concert with cortisol, which has the highest level in the morning while melatonin has its highest level in the evening and during the night. Melatonin also regulates the menstrual cycle and determines when women get into menopause.

Lately new information has come to the forefront showing that there are connections to Alzheimer’s disease, Parkinson’s disease, stroke size and recovery from strokes. Even traumatic brain injury can be minimized when enough melatonin is present. In addition melatonin is an important anti-oxidant.

Finally, there is evidence that melatonin helps to determine how well we age.

In the following I like to review some of the evidence for all of these claims.

1. Melatonin as a hormone

Melatonin levels were found to be very low in breast cancer and prostate cancer patients. It has been determined that the immune cells have melatonin hormone receptors and need melatonin for stimulation. Because of the immune stimulatory effect of melatonin, it is often given as a cancer adjuvant treatment to other cancer treating modalities. Ref. 1 describes that melatonin regulates the female hormones (LH, FSH), which then determine when a woman has her menstrual period and also when she eventually enters menopause. The pineal gland is the master gland for the diurnal hormone rhythms.

Melatonin More Than A Sleeping Aid

Melatonin More Than A Sleeping Aid

2. Melatonin levels decline with age

Melatonin levels in both men and women decline as we age. This figure shows that the highest melatonin levels are reached by the age of 10; by the age of 40 only 15% of the youthful levels remain while by the age of 55 only 5% or less of the original youthful levels are left. This explains why older people are more prone to infections (missing immune stimulation) and why the sleep pattern in older people is changed (shorter periods of sleep, less restful sleep). Ref. 1 points out that with insulin resistance (from diabetes or due to excessive sugar and starch consumption) cortisol levels are chronically elevated, which in turn inhibits melatonin production.

3. Melatonin protects from neurodegenerative diseases

A newer application of melatonin is as a preventative in the neurological field, particularly in the area of Alzheimer’s disease, Parkinson’s disease and the prevention of strokes. With respect to Alzheimer’s disease studies have shown that patients with Alzheimer’s have much lower melatonin blood levels when compared to age matched normal controls. In ischemic stroke patients it was found that stroke patients had much lower melatonin levels when compared to normal age-matched controls. Other studies have shown that pineal gland calcification was associated with low melatonin levels and a high risk for ischemic stroke. This risk was even higher when the patients had high blood pressure, diabetes and high cholesterol/triglycerides. When a stroke has occurred, it is important that the free radicals are removed as quickly as possible, which is where the antioxidant properties of melatonin fit into a rehabilitative program. The presence of melatonin enhances brain plasticity. However instead of using melatonin after a stroke, it is much better to use melatonin regularly before a possible stroke, as this gives a better chance reducing the size of the stroke. This in turn will lead to a faster and more complete recovery after a stroke.

Another important disease of the elderly is Parkinson’s disease. Melatonin helps to prevent oxidative damage to the dopamine producing cells in the basal ganglia thus preventing Parkinson’s disease. As with Alzheimer’s disease, there is a correlation of low melatonin levels and this neurodegenerative disease, which goes beyond the age-related reduction of melatonin levels. In experimental Parkinson’s disease models in mice melatonin was highly effective in preventing deterioration of Parkinson’s disease.

4. Melatonin may extend life

The combination of being a free radical scavenger, an immunostimulant and an integral key hormone allow melatonin to have beneficial effects in the aging process. When melatonin supplements are given, the stimulation of the immune system can cut down infection rates in the elderly, prevent and mitigate degenerative diseases of the brain (Alzheimer’s, Parkinson’s), re-establish sleep/waking rhythms and help reduce arthritis.


Melatonin is a widely used sleep aid. As it is practically absent in people beyond the age of 55, it makes sense to supplement with melatonin in that patient group. However, there are side effects particularly in people on blood thinners as coumadin competes with melatonin in getting eliminated through the cytochrome P450 liver enzyme system. This will result in longer bleeding times in patients on blood thinners who also take melatonin supplements. It is important that patients discuss this with their doctors. However, given all of the benefits described above, for the vast majority of the baby boomers melatonin supplementation would be very beneficial. Doses as a sleep aid vary between 1mg and 5mg at bedtime for most people. Cancer patients require higher doses (10 to 20 mg per day).

More information on melatonin, which is at the center of the circadian hormone rhythm as the key hormone switching from day to night and welcoming the day by switching its secretion from the pineal gland off in the morning: https://www.askdrray.com/how-to-cope-with-time-switches/


1. Datis Kharrazian: “Why isn’t my brain working?” Copyright 2013, Elephant Press, Carlsbad, CA, USA (pages 306-310).

Last edited Nov. 7, 2014