SpectraCell Blog

Lipoprotein(a): An Important Risk Factor for Heart Disease

Posted by Nichole Herms on Fri, Feb 16, 2018 @ 03:32 PM

 

Most people assume that standard cholesterol testing offers an adequate assessment of heart disease risk. If you, like many, have never heard of a lipoprotein profile test, you may be surprised to learn that this test assesses an important risk factor called Lipoprotein(a) or Lp(a) (“lipoprotein little a”). Influenced by genetics and strongly linked to heart disease and blood clotting problems, this risk factor unfortunately is NOT part of routine cholesterol tests or standard lipid panels. In fact, lipoprotein(a) is so strongly linked to heart disease, that it is one of the four lipid-related risk factors cited by the National Institutes of Health National Cholesterol Education Program (NCEP) as worthy of monitoring. Unfortunately, Lp(a) has been notoriously difficult to treat pharmacologically, as statins have shown little efficacy in lowering Lp(a) levels.

Why is Lp(a) so harmful?
Evidence suggests that Lp(a) may serve as the link between thrombosis and atherosclerosis. Recent clinical studies have implicated Lp(a) as a risk factor for blood clots whether or not atherosclerosis is present. Because Lp(a) is a small, very dense LDL, it can easily penetrate the arterial lining, become oxidized and build plaque, thus contributing to atherosclerosis independent of its thrombotic potential. 

How is high Lp(a) treated?

In a recent double-blind, placebo-controlled trial, patients with elevated cholesterol and elevated Lp(a) were divided into two groups, each with 29 people: Group 1 received a statin only and Group 2 received the same statin plus 2 grams/day of L-carnitine, a supplement that plays a key role in fatty acid transport within cells. After 12 weeks, the group receiving only a statin showed about a 7% reduction in Lp(a), but the group receiving the L-carnitine in conjunction with the statin demonstrated over 19% reduction in Lp(a) levels. Authors suggest that co-administration of L-carnitine (whose primary function is fatty acid metabolism), may enhance efforts to lower Lp(a) compared to using a statin alone.

Although heredity plays a large role in the levels of Lp(a), treatment with niacin has also been found to lower levels of Lp(a). 

For additional reading refer to the abstract L-Carnitine/Simvastatin Reduces Lipoprotein (a) Levels Compared with Simvastatin Monotherapy: A Randomized Double-Blind Placebo-Controlled Study published in the January 2017 issue of Lipids

Topics: lipoprotein particle profile, Heart Disease, cardiovascular disease, Lipoprotein Particles, Lipoprotein(a), L-carnitine, Lower Lipoprotein(a), High Lipoprotein(a)

Fasting-Mimicking Diet Helps You Eat Your (Own) Heart Out - Reducing Cardiovascular Disease

Posted by Kirstin Keilty, MS, CNS on Fri, Feb 09, 2018 @ 11:00 AM

FMD-1.jpgAs we stroll into heart month (Feb), still the #1 killer of Americans - 20 years after the declaration to reduce heart-related deaths - here we are. Still. Trying like heck to reduce the risk of heart-related (and other co-morbidities) incidences.

According to statistics from the CDC in 2016, 610,000 heart-related deaths occur each year and it is the leading cause of death in both men and women. That is 1 in 4 Americans.

Why are we still here? After all, we know what we can do: exercise more, take our multivitamin, get regular checks-ups at our doctors' office and - oh yeah - eat more healthfully. Many of us are still sticking to our New Year's Resolutions!

Amid our plight to prepare more healthy home-cooked meals with an eye to consuming higher amounts of plant-based foods, with greater amounts of heart-protecting fiber, healthy, lean proteins, less sugar and processed foods, are we able to keep on with these habits - forever?

Some might say a resounding, "YES!", well, others...maybe...not so much. We have the statistics to prove it.

What do we do if we feel like we have "tried it all", and the results don't appear to be paying off?

What if we have test results, like an advanced lipoprotein or cardiometabolic profile that continue to stare us in the face and prove the errors of our ways? It's disheartening when the labors of our actions appear to be largely ignored by our body's metabolism.

Is it time to finally give up? Should New Year's Resolutions focus on some other aspect, other than finally getting healthy?

Perhaps it is time for a different approach…

The practice of fasting has had many surges over the millennia, extending from times of scarcity, to practices of mystics and religious groups and holidays to health-faddists. Some believed it brought spiritual enlightenment, or quick weight loss; while others believed it gave the digestive system a chance to rejuvenate itself, similar to the idea that adequate nightly sleep allows a reset of the nervous system.

It is largely this last assumption which has pioneered continued research into fasting and its multiple health benefits, including heart (but not limited to) health.1-4

I had the good fortune of learning first-hand about the incredible research into fasting this past December while attending the American Academy of Anti-Aging Medicine in Las Vegas. Valter Longo, PhD, who directs the USC Longevity Institute, expertly presented his research on fasting and its connection to a longer, healthier existence.5 Instead of fasting for long periods of time (4 days to a couple of weeks), the same benefits can be achieved through "Time-Restricted Fasting/Re-feeding" (TRF) or "Fasting-Mimicking Diet" (FMD). Below are two links to fascinating presentations featuring Dr. Longo and his work.

BBC Documentary with Longo and Maslow

FoundMyFitness Interview Longo and Rhonda Patrick

Essentially, with TRF and FMD, an individual can positively impact health for prolonged periods of time simply by choosing to consume all of their daily calories in an 8-hour window. If the first caloric consumption (this includes beverages so no cream or sugar in your coffee) of the day starts at 10:00 AM, an individual is done feeding by 6:00 that evening. If 11:00 is start time, 7:00 is finish time, and so forth.

What does FMD do, exactly?

The Fasting-Mimicking Diet creates the time needed to accomplish an "internal housekeeping" on the cellular level known to stimulate a pathway called: autophagy. Whether you choose to say it "Ah-tauf-ah-gee"or "auto-fay-gee" (I've learned both are right), somatic cells auto-phagocytize, literally eat themselves, to sweep out the debris of aberrant (faulty, damaged or maladapted) cells that build up in our cellular metabolism. Additionally, internal organs, like the heart, all shrink to their reset size, which allows for more effective functioning. When we eat too frequently and don't allow the digestive system to rest, clean and rebuild with re-feeding, autophagy processes are disrupted.

How will autophagy improve my heart health, specifically?

As noted earlier, autophagy has profound positive effects on many body systems and functions, as well as cancer prevention and other diseases, but one of the most researched areas in autophagy include cardiovascular disease. Since mitochondria are found in abundance within the cardiac muscle and TRF and FMD precipitate autophagy, another way fasting improves heart health might be through preserving mitochondrial integrity.
6

Dr. Longo's research has also shown that TRF and FMD influences cellular adaptive responses by reducing oxidative damage and inflammation; as well as optimizing energy metabolism and bolstering cellular protection.7

  1. Xie W, Zhou J. Aberrant regulation of autophagy in mammalian diseases. Biol Lett. 2018;14(1).
  2. O'Flanagan CH, Smith LA, McDonell SB, Hursting SD. When less may be more: calorie restriction and response to cancer therapy. BMC Med. 2017;15(1):106.
  3. Choi IY, Piccio L, Childress P, et al. A Diet Mimicking Fasting Promotes Regeneration and Reduces Autoimmunity and Multiple Sclerosis Symptoms. Cell Rep. 2016;15(10):2136-2146.
  4. Brandhorst S, Choi IY, Wei M, et al. A Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and Healthspan. Cell Metab. 2015;22(1):86-99.
  5. Longo VD, Panda S. Fasting, Circadian Rhythms, and Time-Restricted Feeding in Healthy Lifespan. Cell Metab. 2016;23(6):1048-1059.
  6. Traba J, Sack MN. The role of caloric load and mitochondrial homeostasis in the regulation of the NLRP3 inflammasome. Cell Mol Life Sci. 2017;74(10):1777-1791.
  7. Longo VD, Mattson MP. Fasting: molecular mechanisms and clinical applications. Cell Metab. 2014;19(2):181-192.

Topics: Cardiovascular Health, Heart Disease, Heart Health, Fasting-Mimicking Diet, FMD, FMD Helps Reduce Cardiovascular Disease, Autophagy, Cellular Metabolism

Clearing Up the Cholesterol Confusion

Posted by SpectraCell Laboratories, Inc. on Thu, Feb 01, 2018 @ 01:52 PM

heart apple.jpgConsider this startling statistic: 50% of people who have heart attacks have "normal" cholesterol.  Stated differently, half of all heart attack victims could have a routine cholesterol test done on the very day they have a heart attack and their cholesterol (by routine testing standards) would be "normal" range. So, why do so many practitioners use a diagnostic test that is only 50% accurate?  The reason is simple:  it’s the test with which they are familiar and have been using for decades.  Knowing your HDL and LDL - the "good" and "bad" cholesterol is only the beginning.  SpectraCell’s LPP (Lipoprotein Particle Profile) test goes much, much further.
 
Here is the basic scenario of heart disease:  When our blood vessels are "scratched," or injured, plaque builds up in our arteries to repair the injury, sort of like a scab on the inside of  the blood vessel, causing reduced blood flow. Since plaque buildup is our bodies' response to injury of the blood vessels, reducing the injury to our arteries is key.  
 
That's where cholesterol comes in. Cholesterol is actually a response to vascular injury - not the cause of it. Cholesterol is really not the culprit. Lipoproteins are. Lipoproteins are what "scratch" or "burrow" into our arteries causing injury.  They are actually tiny balls in our blood that carry the cholesterol, our vascular scapegoat. Lipoproteins are what do the damage, not the cholesterol inside them. Cholesterol is really just along for the ride. Lipoproteins, at least the dangerous ones, are the real villain.
 
There are different sizes of lipoproteins. In general, bigger is better.  Here's why: Larger, fluffier LDL particles cannot lodge into your arteries (which is an injury to the artery) as easily as the smaller LDL particles can. Less injury to the artery means less plaque formation and clearer, more pliable blood vessels - a good thing. So it is imperative to understand what kind of LDL (low density lipoproteins) you have floating around in your blood. There are some that are extraordinarily dangerous and some that are completely benign.
 
For example, RLP (also called remnant lipoprotein) has been cited by the government as a very high risk factor for heart disease. But statins, which lower LDL, will do nothing to help your RLP, which are best lowered by high dose omega 3 fatty acids. So, if you don't know what kind of lipoproteins you have, you're shooting in the dark in terms of what treatments you should take. You can see why measuring just plain old cholesterol is certainly not enough. That is why 50% of the people who have fatal heart attacks have "normal" cholesterol - they are not getting the right cholesterol/ lipoprotein test done.
 
Here's the best part:  SpectraCell's LPP® test costs about the same as an outdated cholesterol test and it is also often covered by insurance. Why wouldn't you want an LPP® done?

Topics: Cholesterol, Heart Disease, Heart Attack, Heart Health, Lipoprotein Particles, LDL and HDL, HDL, Standard Cholesterol Testing, Lower LDL, Plaque Formation

Is the Lack of Carnitine a Root Cause of Autism?

Posted by SpectraCell Laboratories, Inc. on Tue, Dec 05, 2017 @ 11:00 AM

autism.jpegAlthough autism likely has more than a singular cause, it is possible that one nutrient deficiency or imbalance can have a significant impact on its development. Recent evidence suggests that carnitine – a relatively under-recognized nutrient among the general public – plays a bigger role in autism than previously thought.

Carnitine’s main function is to transport fatty acids into the cellular powerhouse (mitochondria) for energy. Low carnitine status (common in autism) can impair the ability to use fatty acids for learning and social development.  This recent research hypothesizes that carnitine deficiency may cause symptoms of autism and goes on to suggest that up to 20% of autism cases may be preventable via appropriate supplementation. The author points out that a defect in carnitine biosynthesis is a risk factor for autism, citing the gene (SLC6A14) that limits carnitine utilization in the brain. Expressed only in males, this suggests the reason that autism is more prevalent in boys than in girls. 

For additional information about the micronutrient impact on this this condition, download the Nutrients and Autism flyer here.

For more details on the cited paper, click here for a link to the abstract, “Brain carnitine deficiency causes nonsyndromic autism with an extreme male bias: a hypothesis,” published in the July 2017 issue of Bioassays

Topics: micronutrients, nutrition and autism, micronutrient status, Carnitine Deficiency and Autism, Nutrient Deficiency, Low Carnitine Status

Vitamin B1 and Female Fertility

Posted by SpectraCell Laboratories, Inc. on Wed, Nov 29, 2017 @ 11:00 AM

pregnant.jpegA vitamin B1 deficiency has been shown to compromise egg cell health in female mice. Even though this study was carried out on mice, the implications for human health and fertility are not lost. Scientists were interested in assessing the effect of mild and severe vitamin B1 (thiamin) deficiency on egg cells and what they found was revealing. 

Mice were fed one of two diets: normal or one lacking in vitamin B1. Not surprisingly, the vitamin B1 concentration in the ovaries of mice not given vitamin B1 was much lower than that of mice fed B1. Since the major source of cellular energy in oocytes (immature egg cells) comes from a compound (pyruvic acid) that is metabolized by a vitamin B1-dependent enzyme, researchers wanted to investigate the impact of B1 deficiency on egg cell development. 

If the vitamin B1 deficiency was “mild” (not severe enough to cause weight loss), the mice ovaries produced egg cells that were normal. However, if B1 deficiency reached severe levels, then their ovaries would produce abnormal egg cells more often: 44% of eggs from severely deficient animals were abnormal, compared to only 14% of eggs from mice with adequate B1. Furthermore, once the mice returned to a vitamin B1-containing diet, the level of abnormal egg cells dropped from 44% to 23%, suggesting that egg cell damage may occur as the cell matures but not in its immature stage. 

For more details on the cited paper, click here for a link to the abstract, “Effects of Mild and Severe Vitamin B1 Deficiencies on the Meiotic Maturation of Mice Oocytes,” published in the March 2017 issue of Nutrition and Metabolic Insights.  For a copy of the full paper, click here

Topics: micronutrients, Vitamin B1, Vitamin B1 and Fertility, Female Fertility, Vitamin B1 Deficiency

Vitamin K May Boost Performance in Athletes

Posted by SpectraCell Laboratories, Inc. on Tue, Nov 21, 2017 @ 11:00 AM

cyclist-1.jpegVitamin K is often regarded as a nutrient for improving heart health, lowering cancer risk, and increasing bone density, but it also appears to improve fitness even in healthy athletes. Like most nutrients, it seems to have quite versatile roles.

In this small study, 26 trained male and female athletes were administered placebo or vitamin K2 supplements for eight weeks while they maintained their regular exercise routines. At the beginning of the study and after eight weeks, each person completed a fitness test on an exercise machine designed to quantify their physical work load, oxygen consumption, respiratory rate, cardiac output, and heart rate.  

Vitamin K2 supplementation was associated with a 12% increase in cardiac output (volume of blood that the heart is capable of pumping per beat). The authors suggest that vitamin K2, which has previously been shown to play a role in energy metabolism (especially in tissues with high energy requirements such as skeletal muscle and heart) might be considered in healthy athletes to improve performance. 

For more details on the cited paper, click here for a link to the abstract, “Oral Consumption of Vitamin K2 for 8 Weeks Associated With Increased Maximal Cardiac Output During Exercise,” published in the July 2017 issue of Alternative Therapies in Health and Medicine. 

Topics: micronutrients, Vitamin K, Nutrition, Nutrition and Sports Performance, Vitamin K and Sports Performance, Vitamin K and Heart Health

Can We Change Our Genetic Expression with Nutrients?

Posted by SpectraCell Laboratories, Inc. on Fri, Nov 17, 2017 @ 11:30 AM

DNA Human.jpgRecent evidence suggests that the answer is yes.  Most people understand that we all have inherent genetic predispositions – some as benign as the shape of our nose and others more dangerous such as the tendency toward certain cancers.  However, as research on epigenetics grows, the ability to modulate the expression of certain genes is becoming clearer.  Epigenetics is the study of how our genetic expression is affected by factors other than changes in DNA sequence.  These factors include our environment, including what we eat, supplements we take, toxins, illnesses, even the amount of sunlight to which we are exposed. 

In this study, variations (known by geneticists as polymorphisms) in a specific gene that makes a protein called the zinc transporter 8 (ZNT8), which carries zinc into the hormone insulin, were studied. This protein ZNT8 is responsible for ensuring that pancreatic beta cells (the cells that make insulin which allows us to metabolize blood sugar) have adequate zinc available.  If cells in the pancreas do not have enough zinc, they will not function optimally which may ultimately result in higher risk of insulin resistance and the metabolic dysfunction that follows.  

When participants with the (CC) genotype ingested more zinc and omega 3 fatty acids, they lowered their risk of metabolic syndrome consequences associated with their genotype. Stated differently, people with this specific genotype (CC) responded well (in terms of improved insulin sensitivity and metabolic health) to higher levels of zinc and omega 3 fatty acids, while other genotypes (CT or TT) did not show a meaningful improvement in metabolism.  Since over-supplementation has potentially negative consequences (too much zinc can cause copper deficiency, for example), knowing your genotype may lead to more informed supplementation decisions. 

For more details, click here for a link to the abstract entitled Some dietary factors can modulate the effect of the zinc transporters 8 polymorphism on the risk of metabolic syndrome published in the May 2017 issue of Scientific Reports  (Abstract 2640).  Or read the full paper here.  (Full paper 829)

 

Adapted from July 2017 Clinical Updates.  9/27/2017.  (NLH)

Topics: micronutrients, Epigenetics, Gene Expression, Gene Expression and Nutrition, Genetic Predisposition

One-Third of Americans Have at Least One Micronutrient Deficiency

Posted by SpectraCell Laboratories, Inc. on Tue, Sep 19, 2017 @ 04:03 PM

Using data from the government-sponsored research program National Health and Nutrition Examination Survey (NHANES), a group of researchers compiled data on seven vitamins from over 15,000 people in the US. They determined that 31% of the American population is at risk for at least one vitamin deficiency; 23% of Americans are at risk for deficiency in at least two vitamins, and 6% are at risk for three or more vitamin deficiencies.

The data came from a variety of sources: dietary recall, reported supplement use, and lab results – some information less quantifiable than others. Researchers concluded that the most common vitamin deficiency in the United States is vitamin B6, of which a staggering 20% of Americans are deficient. However, scientists concede that biomarkers of nutrient status are affected by inflammation, suggesting that deficiency rates may be even higher. In addition, nutrient status did not correlate with dietary intake (according to their data), which is not surprising given that determining specific deficiencies via dietary intake is notoriously difficult to quantify. Dietary recall is rarely accurate; even if intake is measured with precision (this is difficult to do and therefore unlikely), absorption of said nutrients is an entirely different problem (itself nearly impossible to assess). A review of the available literature supports the view that a one-size-fits-all approach to micronutrient requirements is both outdated and inaccurate.  

The investigators stated that “sub-clinical deficiency symptoms for many vitamins and minerals are non-specific, and may include fatigue, irritability, aches and pains, decreased immune function, and heart palpitations,” all of which further complicate the quantification of micronutrient deficiency. Functional measurement of intracellular micronutrient status may gain attention as studies like this are published.

For details, click HERE for a link to the abstract. Read the full paper HERE.

Topics: Nutrition, micronutrient deficiency, micronutrient status, vitamin B6 deficiency, sub-clinical deficiencies, intracellular micronutrient status

Leptin Resistance: Everything You Need to Know

Posted by SpectraCell Laboratories, Inc. on Wed, Aug 09, 2017 @ 02:26 PM

Overeating.jpgLeptin, often called the “satiety hormone,” is an adipokine (signaling molecule produced by fat cells) whose main function is to regulate energy and fat stores. In a metabolically healthy person, a temporary increase in caloric intake (such as after a big meal) corresponds to an increase in leptin production. This prompts the hypothalamus to send signals that promote satiety, which cues one to stop eating.

Leptin was the first adipokine to be discovered (in 1994) and changed how scientists view fat tissue. Fat stores were previously thought to be inert tissue that did not cause any direct harm. Upon the discovery of leptin and its related genes, scientists learned that excess adipose tissue is actually metabolically active, releasing several hormones (adipokines) and inflammatory enzymes. Consequently, it is now considered an endocrine organ.

Although leptin suppresses appetite, one can become leptin resistant, feeling hungry even when one consuming enough calories to maintain metabolic requirements. In a way that is analogous to insulin resistance, leptin resistance occurs in obesity: the higher the fat stores, the more leptin produced. In fact, leptin varies exponentially (as opposed to linearly) with adipose tissue. This means that changes in fat mass profoundly affect leptin levels. Over time, as leptin increasingly circulates in blood, the brain eventually becomes resistant to its effects. As a result, one becomes inclined to overeat, unable to experience satiety and therefore feeling hungry even when leptin levels are high! This is referred to as leptin resistance. 

An increase in leptin (in the short term) follows an increase in caloric intake. This promotes satiety and signals one to stop eating. However, in the long term, a chronic increase in leptin can be attributed to excess body fat, estrogen (endogenous and exogenous), insulin (leptin is released dose-dependently in response to insulin), stress, and some steroid medications such as dexamethasone.

Loss of fat tissue, reduction in caloric intake via dieting and fasting, testosterone (which is anabolic – this increases appetite), and ghrelin (the hunger hormone) are all factors that lower leptin. Sleep deprivation, which upregulates appetite, is a reason why sleep loss is linked to cravings, and also impacts levels.

Factors that impact leptin sensitivity include:

  • Excess body weight
  • High Fructose Corn Syrup (this blocks leptin receptors)
  • High Triglyceride levels block leptin’s ability to reach the hypothalamus
  • Estrogen deficiency: the leptin-estrogen link may cause menstrual cravings
  • Lectins in grains bind to leptin receptors, inducing leptin resistance 

Leptin receptors are found in several tissues besides the hypothalamus, including endothelial, muscle, placental, and liver cells. Although its appetite-regulating effects are well established, it is known to play a role in fertility and puberty; however, its other functions are not fully understood.

SpectraCell’s CardioMetabolic test offers a clinically relevant evaluation to help define risk for atherosclerotic cardiovascular disease (ASCVD), progression toward Type 2 Diabetes, and inflammation.
Whether you are at high risk of heart disease or managing an existing metabolic condition, SpectraCell’s CardioMetabolic test is appropriate and recommended.

 GET TESTED

Topics: cardiometabolic, Weight Management, Leptin, Leptin Resistance

Vitamin A: Functions and Benefits

Posted by SpectraCell Laboratories, Inc. on Mon, Jul 31, 2017 @ 11:30 AM

vit A.jpgVitamin A was one of the earliest vitamins to be discovered – hence its top rank in the alphabetical vitamin nomenclature.Vitamin A is a family of fat soluble compounds that play an important role in vision, bone growth, reproduction, and immune system regulation. Most people associate vitamin A with carrots, and for good reason: the common orange veggie has high amounts of beta-carotene, which is actually a vitamin A precursor and also the reason carrots got their name. But vitamin A is actually a group of chemicals that are similar in structure, and include retinol (the most biologically active form of vitamin A), retinal, and retinoic acid.

β-carotene is slightly different in that it is cleaved in the intestinal mucosa by an enzyme to form retinol. Other carotenoids include lycopene and lutein but, although similar to vitamin A, they are not actually vitamin A in the truest sense. One distinction is that excessive amounts of vitamin A from over-supplementation, can cause toxicity (although deficiency is much more common). On the other hand, β-carotene does not cause vitamin A toxicity because there exists a regulatory mechanism that limits vitamin A production from beta carotene when high levels are ingested.

A large number of physiological systems may be affected by vitamin A deficiency which is most often associated with strict dietary restrictions and excess alcohol intake. Patients with Celiac disease, Crohn’s disease and pancreatic disorders are particularly susceptible due to malabsorption.  Vitamin A is also essential for the developing skeletal system and deficiency can result in growth retardation or abnormal bone formation. 

The functions of vitamin A are very diverse:

  • Eyesight: Vitamin A forms retinal, which combines with a protein (rhodopsin) to create the light-absorbing cells in the eye. This explains why a common clinical manifestation of deficiency is night blindness and poor vision.
  • Skin: In addition to promoting healthy skin function and integrity, vitamin A regulates the growth of epithelial surfaces in the eyes and respiratory, intestinal, and urinary tracts. Deficiency impairs epithelial regeneration, which can manifest as skin hyperkeratization, infertility, or increased susceptibility to respiratory infections.
  • Anemia: Vitamin A helps transfer iron to red blood cells for incorporation into hemoglobin; thus, a vitamin A deficiency will exacerbate an iron deficiency.
  • Weight management: Vitamin A reduces the size of fat cells, regulates the genetic expression of leptin (a hormone that suppresses appetite), and enhances the expression of genes that reduce a person’s tendency to store food as fat.
  • Cancer prevention: Vitamin A deficiency impairs the body’s ability to launch cell-mediated immune responses to cancer cells. Vitamin A inhibits squamous metaplasia (a type of skin cancer) and inhibits breast cancer cell growth.
  • Fertility: Vitamin A plays a key role in the synthesis of sperm.
  • Autism: Vitamin A is part of the retinoid receptor protein (G-alpha protein), which is critical for language processing, attention, and sensory perception. Some autistics have a defect in this protein that vitamin A supplementation can modulate.
  • Sleep: Vitamin A deficiency alters brains waves in non-REM sleep, causing sleep to be less restorative.

Vitamin A also interacts with other micronutrients. For example, zinc is required to transport vitamin A into tissues, so a zinc deficiency will limit retinal binding protein (RBP) synthesis and thus limits the body’s ability to use vitamin A stores in the liver. Oleic acid, a fatty acid found in olive oil, facilitates the absorption of vitamin A in the gut.

Find out if you have a vitamin A deficiency, and take steps to correct it, by ordering a micronutrient test today. 

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Topics: micronutrients, Vitamin A, Vitamins, Fertility, Cancer Prevention, Celiac Disease, Supernutrients, Weight Management, Vitamin A Deficiency, Chron's Disease, Anemia, Nutrients, β-carotene