I have a new paper that was published online in FASEB Journal on how vitamin D increases serotonin synthesis in the brain, where it is important for cognition, and decreases it in the gut, where in excess it causes inflammation. Here is a quick summary of the findings of my paper.

Vitamin D is converted into a steroid hormone that controls the expression of over 900 genes in the body, many of which are in the brain. We show that serotonin, oxytocin, and vasopressin, three brain hormones that affect social behavior, are all activated by vitamin D hormone. Autism, which is characterized by abnormal social behavior, has previously been linked to low levels of serotonin in the brain and to low vitamin D levels but no mechanism has linked the two until now. In this study, we show that vitamin D hormone activates the gene that makes the enzyme tryptophan hydroxylase 2 (TPH2), that converts the essential amino acid tryptophan, to serotonin in the brain. This suggests that adequate levels of vitamin D may be required to produce serotonin in the brain where it shapes the structure and wiring of the brain, acts as a neurotransmitter, and affects social behavior. We have also found evidence that the gene that makes the enzyme tryptophan hydroxylase 1 (TPH1) is inhibited by vitamin D hormone, which subsequently halts the production of serotonin in the gut and other tissues, where when found in excess it promotes inflammation.

This mechanism explains many of the known, but previously not understood, facts about autism including: 1) the “serotonin anomaly” low levels of serotonin in the brain and high levels in the blood of autistic children; 2) the preponderance of male over female autistic children: estrogen, a similar steroid hormone, can also boost the brain levels of serotonin in girls; 3) the presence of autoimmune antibodies to the fetal brain in the mothers of autistic children: vitamin D regulates the production of regulatory T-cells via repression of TPH1. Our mechanism is relevant to the prevention of autism, and likely its treatment.

The current guidelines for adequate vitamin D levels are concentrations above 30 ng/ml. Most American’s vitamin D is made in the skin from exposure to UVB radiation; however, melanin pigment and sunscreen inhibit this action. This is a an important cause of the well known widespread vitamin D deficiency among dark-skinned Americans, particularly those living in Northern latitudes. The most recent National Health and Examination survey reports that greater than 70% of U.S. population do not meet this requirement and that adequate vitamin D levels have plummeted over the last couple of decades. This precipitous drop in adequate levels of vitamin D in the US is concurrent with the rise in autism rates.

There is little vitamin D present in food and fortification is still inadequate as is the amount in most multivitamin and prenatal supplements. Vitamin D supplements are inexpensive and offer a simple solution to raise vitamin D levels to an adequate status. In addition, vitamin D levels should be routinely measured in everyone and should become a standard procedure in prenatal care.

In this video, Dr. Rhonda critically analyzes the headline-grabbing editorial entitled: Enough is Enough: Stop Wasting Money on Vitamin and Mineral Supplements, which asserts that vitamin and mineral supplementation is useless or harmful.

http://www.youtube.com/watch?v=o0u8UdZeOhc

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Check out my guest blog post on WellnessFX on how there is a trade off when it comes to growth hormone and IGF-1. Growth hormone and IGF-1 enhance muscle and cognitive performance but this comes at a cost: longevity. Reduced growth hormone and IGF-1 increase lifespan by increasing the expression of genes involved in stress resistance but at an expensive cost when it comes to muscles and brain. Learn all about the trade-off and ways to circumvent it.

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Check out my guest blog post on wellnessFX on how vitamin D regulates the aging process. I discuss important factors that affect vitamin production from your skin, what the optimal levels of serum vitamin D are, and how appropriate vitamin D levels (“the sweet spot”) prevents telomeres from shortening.

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Check out my guest blog post on WellnessFX on the 3 main causes of magnesium deficiency in the US and how you can avoid becoming deficient.

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Check out my guest blog post on WellnessFX on how magnesium will help boost your mitochondria to enhance your exercise performance.

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Disruptions in the body’s circadian rhythm, the 24-hour cycle that regulates sleep, wakefulness, metabolism, and other physiological processes can have major health consequences. It has long be known that the brain contains a central circadian clock which is located in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus in the brain. Over the past few years accumulating evidence has revealed  that every single organ, tissue, and cell in your body has its own circadian clock and the brain acts to keep all the different circadian rhythms in sync.  These circadian clocks operate at maximum efficiency at certain times of the day, so disturbing your cells’s circadian rhythms by:

• eating at the wrong time of day
• drinking caffeinated beverages too late in the day
• just generally getting too little sleep

can send your internal clocks out-of-whack, causing major a disruption to your body’s physiological processes. For example, if the circadian rhythm in your pancreas is out of sync with your liver, this can throw off the timing between these two important systems causing your pancreas at any given moment to produce too little or too much insulin leading to eventual type 2 diabetes. This fact was demonstrated in mice by perturbing the circadian clock in the pancreas, causing type 2 diabetes.

Disruption of The Circadian Clock By What Time of Day We Eat and What We Eat

Knocking-out a gene that controls the internal clock in the pancreas is one thing, but what about disruption of the circadian clock by what time of day we eat or what we eat? Well, mice that were fed a high-fat diet, changed the expression of circadian-clock genes the brain, the liver and in fat tissue, thus, sending these internal clocks out of sync. In addition, nocturnal mice that sleep during the day and are awake at night were fed  a normal diet during the day, when they usually sleep. The end result: the mice became obese.

Well these are mice! What about humans?

A new study in humans had similar findings: people that sleep fewer hours tend to eat late at night and pack on the pounds easier.

The bottom-line is this: our bodies exist in a constant amazingly dynamic equilibrium with all sorts of environmental variables: neglecting any one (or many) variables — such as sleep or diet — can lead to consequences that extend beyond that which common sense would dictate we should expect.

References:
Kohsaka A, Laposky AD, Ramsey KM, Estrada C, Joshu C, Kobayashi Y, Turek FW, Bass J. High-fat diet disrupts behavioral and molecular circadian rhythms in mice. Cell Metab. 2007 Nov;6(5):414-21. PMID: 17983587.

Turek FW, Joshu C, Kohsaka A, Lin E, Ivanova G, McDearmon E, Laposky A, Losee-Olson S, Easton A, Jensen DR, Eckel RH, Takahashi JS, Bass J. Obesity and metabolic syndrome in circadian Clock mutant mice. Science. 2005 May 13;308(5724):1043-5. PMID: 15845877.

Spaeth A, Dinges D, Namni G. Effects of Experimental Sleep Restriction on Weight Gain, Caloric Intake, and Meal Timing in Healthy Adults. Sleep. 2013 July;36 (7).http://dx.doi.org/10.5665/sleep.2792

Video, part I

Nobody wants cancer. Cancer is one of the most painful terminal diseases that, in some cases, can go on for years with limited conventional treatment options that are often just as painful, if not more, than the cancer itself. These conventional treatment options often consist of a standard checklist of options, often with grim side effects, that most medical physicians check off one-by-one, without a second thought or reconsideration.

What if I told you there was a way to likely dramatically decrease the risk of you and your loved ones from becoming victim to this devastating disease? The obvious scenarios aside, such as smoking or standing in UV sunlight for prolonged periods of time without any protection, your diet is the #1 way you can control your cancer risk.

You’ve heard it before: “Eat your dark green vegetables and your fruits if you want to be healthy.” But there is so much more hidden in this little fact that is so important, in fact, I’m going to break it down for you in a easily digestible manner so that you can understand the true meaning of that so often quoted sentence.

Let’s start at the beginning. What causes cancer? Cancer is most definitely a disease of age, cancer risk increases exponentially by the age of 50. So why does it so often take long to get cancer and why do some people get it earlier than others? Well, those of us that were lucky to not have been born with any mutations in genes that can cause cancer in childhood are lucky to some degree, but we are not in the clear. So if you are not born with mutations what else can cause mutations? Mutations are formed when there has been damage to your DNA. DNA damage can be in the form of oxidation or a break in the DNA strands. Every cell in your body has DNA and this DNA makes up thousands of different genes. Every organ in your body is made up of tissue that is made up of cells. The cells in your skin, lungs, liver, pancreas, kidney, bladder, breast, prostate (you get the point) all have DNA within each cell.
Let’s summarize this because it is pretty fundamental.

• Every organ in your body is made up of millions of cells.
• Every cell that makes up your organs contains DNA.
• The DNA inside every single one of your millions of cells makes up your genes.
• The genes are what control processes inside your body.

These cells inside each organ have a limited lifespan and replicate to produce daughter cells that contain the exact DNA. This daughter cell will then replace it’s mother cell so that it can live for a certain amount of time to do it’s function before repeating the same process. For example, the cells in your kidney help maintain blood pressure and help filter toxins out of your blood. This is the function of the millions of cells that make up your kidney. The genes that make up the DNA inside those kidney cells are what control whether those important functions (blood pressure and filtering toxins from the blood) are performed properly. In other words, your DNA inside your kidney cells has to be healthy for those cells to do their job.

It all seems pretty straightforward, your cells reproduce to make exact copies of themselves so that the organ can continue to do its job. But in order for this to happen the DNA from the cell has to be copied to make a new cell. This usually happens with ease, well, unless the DNA has been damaged, and the damage is not repaired. In this case, the cell replicates itself with the damage in the DNA, and now the daughter cell is not an exact copy. It will contain a mutation in a gene that makes up the DNA. Here is the real kicker: that mutation is permanent. It is the point of no return. Once a mutation always a mutation, and the mutation keeps getting passed on to each daughter cell. Let’s summarize because this part is important to understand.

• Cells that make up each organ each have their own important function to carry out.
• Each of these cells have a limited lifespan so they have to make a copies of themselves to ensure the organ will continue to function.
• In order for a cell to reproduce a make an identical daughter cell it must copy all of it’s DNA.
• If the DNA is damaged and that damage is not repaired, then the daughter cell will get a mutation in a gene that makes up the DNA inside the cell.
• A mutation is permanent. There is no repair to a mutation.

At this point, you may be thinking that repairing that DNA damage before it causes a mutation is pretty important, otherwise, there is no turning back. Well, that would be correct. So why doesn’t all damage to DNA get repaired? This part is really important to understand. The act of repairing damaged DNA relies on DNA repair enzymes inside your cells to work efficiently and effectively. But these DNA repair enzymes require energy, vitamins, and minerals to work properly. For example, magnesium is one extremely important mineral that many different DNA repair enzymes need in order to repair damaged DNA. What happens if your magnesium levels are low? Well, then your DNA repair is low, which automatically puts you at an increased cancer risk. Did you know that 56% of the US population is deficient in magnesium? That is because magnesium is found in dark leafy green vegetables, such as spinach, kale, and is also high in almonds as well. If you are not eating a big plate of spinach EVERY DAY, then you likely have inadequate levels of magnesium. Do you think most Americans eat a big plate of spinach on a daily basis? This translates to insidious damage to your DNA that goes unrepaired, thus, causing mutations.

Even if you avoid all the known carcinogens to the best of your ability, you can not avoid cancer-causing damage altogether. Just normal metabolism, the way the cells in your body generate energy, can wreak havoc on your DNA, causing damage and possibly mutations. Just normal living causes DNA damage on a daily basis. You can not avoid it. Our DNA repair enzymes are working really hard to repair that damage so that DNA damage does not translate to mutations. You can think of DNA repair enzymes as guardians of you genome because they guard against cancer-causing mutations. Do you understand why it’s so important to eat your spinach? Okay let’s summarize again because this really needs to be driven home.

• Normal metabolism causes damage to DNA , everyone gets DNA damage to some degree.
• DNA repair enzymes inside your cells repair the damage to your DNA to prevent mutations.
• These DNA repair enzymes require magnesium (as a a co-factor) to work properly.
• If you are low in magnesium, then DNA repair enzymes are not working optimal and may not repair damage to your DNA.
• 56% of the U.S. population is deficient in magnesium.
• Spinach is a rich source of magnesium.

Video, part II

If the DNA can not be repaired the cell will try and execute another mechanism to prevent mutations. The cell will try and sacrifice itself for the greater good by killing itself, sorta of like one final act of altruism. You may have heard this referred to as apoptosis, which literally means programmed cell death. Yes, this self-destruct mechanism that helps kill cells that have those cancer-causing damage, is a genetically-defined program. In case you are confused by that terminology, let me explain it to you. This means that certain genes inside the cell detect that damage has occurred, then the rapidly execute the death of the cell. These genes are often referred to as tumor-suppressor genes because they suppress the formation and survival of cancer cells. There are various organic compounds that are present in vegetables that help increase the gene expression of tumor-suppressor genes so that they more potently do their function of killing any of these dangerous, damaged cells. A prime example are sulforaphanes and isothiocynates, compounds present in the cruciferous family of vegetables including broccoli, kale, cauliflower, cabbage, and brussel sprouts. These two compounds found in cruciferous vegetables have been shown to activate tumor-suppressor genes and kill cancer cells. Do you eat a vegetable from the cruciferous family on a daily basis? If the answer is no, think about reconsidering your diet. Let’s summarize this new information.

• Cells that contain damaged DNA that is not repaired can self-destruct to prevent mutations.
• In order for the damaged cell to die, tumor-suppressor genes have to be activated to kill the cell.
• Sulforaphanes and isothiocynates activate tumor-suppressor genes.
• Sulforaphanes and isothiocynates are organic compounds in cruciferous vegetables.
• Cruciferous vegetables consist of broccoli, kale, cauliflower, cabbage, and brussel sprouts.

There is one problem. If the damage occurs in the part of DNA that contains those tumor-suppressor genes then this may disrupt that gene from working properly. The end result: the cell will get a mutation in the tumor-suppressor gene which is the worst kind of mutation because that gene can no longer eliminate cancer cells so this type of mutation can rapidly lead to cancer, since their role in preventing cancer is so important.

You may be asking yourself what dictates getting a mutation in a tumor-suppressor gene vs. any other gene? Well, the answer is simple. It’s totally random. The more DNA damage you accumulate in your lifetime, the more you increase your risk of that damage occurring in a tumor-suppressor gene.  DNA damage occurs at random places in your DNA, and it often takes decades before you finally get a mutation in a tumor-suppressor gene. This is one important reason why cancer is a disease of age. It’s simple statistics. Each time the damage occurs, it’s a roll of the dice. There are hundreds of thousands of places that this damage can occur on your DNA. Some places hurt more than others. This is why minimizing your exposure to the damage and boosting your DNA repair enzyme activity is so important. A quick summary here.

• Damage and mutations occur at random spots in your DNA (ie. random genes).
• If the mutation occurs at a tumor-suppressor gene, then cancer risk increases exponentially.
• The more damage that occurs to your DNA, the more likely you are to get a mutation in a tumor-suppressor gene.
• DNA damage accumulates with age, this is one reason why cancer is a disease of age.