In a large clinical study called AIM-HIGH (for Atherothrombosis Intervention in Metabolic Syndrome with Low HDL/High Triglycerides and Impact on Global Health Outcomes), researchers evaluated the impact of extended release niacin (vitamin B3) on blood lipids. In a previous review of patients in this AIM-HIGH trial, niacin showed no benefit to statin-treated patients when analyzed as a whole group. However, in a subsequent analysis, niacin appeared to benefit patients who had high triglycerides (over 200 mg/dL) and very low HDL (less than 32 mg/dL). In this analysis, the authors sought to find out the specific changes in lipoproteins that conferred the benefit seen in the subset of patients with high triglycerides and low HDL.
Lipoprotein particles were analyzed on 2457 participants in the AIM-HIGH trial to establish baseline values and again after one year of treatment with extended release niacin. Those taking niacin had higher HDL after one year (a good outcome since HDL is protective). In addition, the analysis of lipoprotein subfractions showed that this benefit – specific to people with high triglycerides and low HDL – was likely due to the reduction in remnant lipoproteins, also known as RLP.
This unique lipoprotein is particularly harmful because unlike LDL particles, which have to undergo oxidation before they can be taken into the arterial intima, RLP lipoproteins can be readily transformed into foam cells which is what comprises arterial plaque. In fact, RLP is one of the four major risk factors cited by the National Cholesterol Education Program that contribute to heart disease. This paper suggests that the benefit seen in patients taking niacin was due to a reduction in this particularly harmful lipoprotein called RLP.
Micronutrients are involved in the body’s countless metabolic reactions; therefore, a single deficiency can affect cardiac and metabolic health. Regardless of your medical history and current health, micronutrient testing in combination with our CardioMetabolic evaluation can help your health care provider identify your risk and design a personalized treatment plan for you.
(Journal of Clinical Lipidology, May 2018)
In this case report, a 41-year-old man who had been suffering from cluster headache since the age of 15 years old was treated with high dose vitamin B1 (thiamine). He had been diagnosed with cluster headache at a neurological center in Italy. His first headache occurred at age 15 shortly after a motorcycle accident and they increased in frequency over the years, with acute pain and intensity that significantly compromised his quality of life. Although the patient would experience some headache free months over the years, in January 2016 the headache clusters began occurring daily with no pain-free period for an entire year. The patient had been treated with sumatriptan, a commonly prescribed drug for cluster headache, which did not work. He had also been prescribed prednisone, although this not alleviate the pain either. In December 2016, he was given oral high dose vitamin B1. Initially, the dose was 250mg, then it was increased to 750 mg after a few days. Within 10 days, the headache pain disappeared. He continued the vitamin B1 daily indefinitely.
Interestingly, the neurological center requested that he stop the vitamin B1 in order to test whether the headaches would come back. He refused this request citing his reluctance to re-experience his headache pain. However, in May 2017 (five months after B1 treatment started), the patient forgot his vitamin B1 while on a vacation. Within 48 hours of the last dose, a painful headache occurred. He resumed vitamin B1 therapy after his vacation and was able to reduce the dose to 500mg with no recurrence of headaches to date.
Cluster headache is a painful condition in which very severe headaches occur with little warning and in “clusters” meaning several headaches will occur in a short time period. Patients of cluster headache have very little or no warning when they occur unlike migraine which may gradually build in intensity. Classified as a neurological condition, cluster headache is characterized by very severe and intense pain around the eye, often on only one side of the head. Some researchers suggest that the role vitamin B1 plays in energy metabolism, brain function and pain modulation make it a potential therapy for this rare neurological disorder.
(Case Reports in Neurological Medicine, April 2018)
LINK to ABSTRACT Oral High-Dose Thiamine Improves the Symptoms of Chronic Cluster Headache.
Previous research has shown that biotin deficiency increases inflammation but since there are so many causes of inflammation – physiologically speaking – the actual metabolic pathways between biotin deficiency and inflammation are unclear. In this study, researchers subjected human immune cells to biotin deficiency and compared the result to human immune cells living in a biotin-rich environment. Biotin, also known as vitamin B7, is a key vitamin necessary for proper cellular metabolism. It is a cofactor to cellular energy production and therefore important to cellular health at a fundamental level.
When the human immune cells were biotin deficient, expression of inflammatory proteins increased. Specifically, CD4+T cells were used, which are also known as T-helper cells because they are a type of white blood cell that directs the function of other immune cells. In other words, T-helper cells supervise immune cells, sending signals to attack viruses and bacteria, for example. In biotin deficiency, the number of these regulatory immune cells (CD4+T) decreased. At the same time, biotin deficiency caused an increase in the metabolic pathway (called mTOR) that regulates cell growth. mTOR (mammalian target of rapamycin) is a protein that senses the nutrient and energy status of cells and regulates their metabolism accordingly. A decrease in mTOR is generally good and can lead to a longer lifespan. An increase in mTOR is generally bad and can lead to tumors or cancerous growths.
The results of this study – both in vivo and in vitro – showed that biotin deficiency increased the mTOR pathway, which then resulted in an increase in several inflammatory compounds. This, combined with the fact that biotin deficiency decreased the number of T-helper cells, meaning fewer immune cells were around to regulate everything, ultimately induced the increase in inflammation seen in biotin deficiency.
(Journal of Immunology, April 2018)
LINK to ABSTRACT Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway.
The prevalence of AD in our aging population is frightening, affecting 10% of those over age 60, 20% of those over age 70, and 30% of those over age 80.1 There are roughly 5 to 6 million AD patients in the US and an equal number of people with mild cognitive impairment (MCI), memory loss, but not enough loss of function to be called AD. In general, MCI is a precursor to AD, with 80% eventually developing AD, at the rate of 15% per year.2
Supplementation with Zinc
Because this was an animal study, researchers could precisely manipulate and consequently correlate blood and brain levels of zinc and copper and with age and cognitive function. Specifically, they measured the effect of zinc supplementation on short-term memory, long-term memory and spatial memory. In addition, they measured zinc and copper levels in both the blood and the hippocampus, which is the part of the brain linked to memory.
The authors discovered that as the rats got older, their blood levels of copper increased while blood levels of zinc decreased with simultaneous decreases in memory. However, supplementation with zinc reversed the elevated copper levels and improved memory in all areas. It is well established that zinc and copper work together and that balance of the minerals is important. In fact, excess zinc supplementation may possibly induce a copper deficiency, so although this study concludes “zinc as a plausible therapeutic intervention” for age-related cognitive decline, this study reminds us that micronutrients do not work alone but in balance so a comprehensive look at nutritional status is key.
Download our Cognitive Function Nutrient Wheel.
1. Alzheimer's Association. Alzheimer's Disease Facts and Figures. 2010:1–74.
2. Oscar L. Lopez, M.D. Mild Cognitive Impairment. NCBI 2013 Apr; 19(2 Dementia): 411–424
LINK to ABSTRACT Supplementation with zinc in rats enhances memory and reverses an age-dependent increase in plasma copper.
Personalized medicine has changed the healthcare paradigm. It is now possible to determine your personal micronutrient needs based on your own cells’ metabolic requirements.
SpectraCell’s Micronutrient Test measures over 30 vitamins and minerals at the cellular level. But the SpectraCell test goes even further – it measures functional, long-term status within the cell – which evaluates how well your body actually utilizes each nutrient. Several factors affect nutrient status – age, lifestyle, genetics, medications, absorption rates, gut health, hormones and more. SpectraCell’s Micronutrient Test embraces this biochemical individuality.
Mineral deficiencies profoundly affect prostate health. Selenium deficiency has been linked to higher levels of prostate specific antigen (PSA), a common biomarker for prostate problems. Interestingly, the epithelial cells in the prostate gland accumulate the highest levels of zinc in any soft tissue of the body and low zinc is linked to prostate inflammation. In the case of prostate cancer, strong evidence suggests higher intake of zinc may improve prognosis. Vitamin K show anti-carcinogenic properties in various cancer cell lines, including prostate cancer cells. Vitamin D also exhibits anti-cancer activity in prostate cells via its role in regulating male hormones. Vitamin C downregulates an enzyme that causes abnormal tissue growth in the prostate gland, thus protecting against a condition known as BPH – benign prostate hyperplasia – which manifests with urination problems in men. Animal studies have shown that Vitamin E may suppress prostate tumor formation. But results on vitamin E supplementation trials and prostate health has been equivocal, suggests that blind supplementation when not deficient, may be harmful. Targeted repletion of actual – not assumed – deficiencies is key.
Chemotherapeutic drugs used in the treatment of testicular cancer can wreak havoc on healthy testicular tissue. Evidence suggests antioxidants can protect against this damage. For example, the antioxidant N-acetyl cysteine has been shown to reverse the damage done by bleomycin, a common drug to treat testicular cancer. Evidence suggests combinations of specific antioxidants (vitamin E, C, zinc, selenium) may lower the risk of testicular cancer from spreading (mestastasizing). Since oxidative stress plays a big role in testicular toxicity, nutrients that acts free radical scavengers are particularly beneficial in the testes. Vitamin C protects the surface of testicular cells. Glutathione protects sensitive testicular tissue from oxidative stress. Mineral cofactors (Zinc, Copper, Manganese) are need to activate powerful protective enzymes active in testes. A single micronutrient deficiency can profoundly compromise man’s ability for healthy cellular detoxification.
Contrary to popular thought, erectile dysfunction is less commonly a problem in hormone levels, and more commonly a problem with vascular health. Several nutrients affect how well a man’s blood vessels respond to chemical cues. Vitamin D’s role in calcium transport affects a man’s vasculature and thus erectile function. Folate and inositol may improve erectile dysfunction by activating nitric oxide, a chemical in the blood that tells vessel to properly dilate. Vitamin E and lipoic acid are necessary cofactors in nitric oxide production, and thus vascular and erectile health. Depending on the presence of certain genes, repletion of folate and vitamin B6 has been shown to benefit men who were non-responsive to sildenafil, a common medication used for treatment of ED. Another study shows carnitine and vitamin B3 improved sexual performance in men with ED. Glutathione depletion will compromise a man’s ability to achieve vasodilation. Any nutrient that benefits vascular health will also benefit erectile health.
The male equivalent of female menopause is andropause, which is a gradual decline in testosterone levels as men age. However, micronutrients profoundly affect testosterone levels. For example, vitamin B6 stimulates the brain to increase testosterone production. Conversely, deficiency in folate reduces circulating testosterone. The rate-limiting enzyme for testosterone synthesis is vitamin K dependent, so a deficiency will lower its production. Magnesium is needed to make testosterone biologically active, freeing it up in the bloodstream so it can act on muscles throughout the body. Vitamin D, which is actually a hormone, is the precursor molecule to testosterone and can significantly increase total and free levels of testosterone throughout the body. Carnitine is directly related to testosterone levels and may prevent testosterone decline after intense physical stress. Depending on baseline levels, zinc and selenium can increase testosterone as well.
STRESS, STRESS and more STRESS
In today’s highly competitive world, men encounter inordinate amounts of stress, particularly in the workplace. Although the physiological effects of chronic stress are often dismissed, the effect of stress on cellular health is indisputable. Micronutrient deficiencies can exacerbate the physiological effects of stress. Conversely, micronutrient repletion can repair stress-induced cellular damage. Serine has been used in the treatment of PTSD (post traumatic stress disorder) as it buffers the negative effects of stress in the body. Folate, choline and inositol directly affect brain chemicals that calm the mind and body. B vitamins serve as cofactors in the production of anti-anxiety neurotransmitters. Micronutrients help stave off the fatigue associated with long term stress. Nutrients such as coenzyme Q10 and magnesium may improve energy in chronically stressed out men. Correcting micronutrient deficiencies can enable men to face daily challenges while minimizing the physiological repercussions.
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Huntington’s disease is a relatively rare disease that occurs when a person has altered expression of a specific gene called the huntingtin gene. The presence of this mutated gene initiates the synthesis of an altered protein (similarly called the mutated huntingtin protein, or mHTT) that damages nerve cells in the brain over time. The disease progresses over the course of several years and clinically manifests as gradually worsening mental, emotional and physical dysfunction, to the point of total incapacity.
In this experiment, scientists studied the effect of supplemental vitamin B1 (thiamine) on B lymphocytes (white blood cells) that carried the mutated Huntington gene and compared them to normal B lymphocytes that did not carry the mutated gene, which served as the control. The scientists supplemented vitamin B1 on the two sets of cells and compared the following: (1) cell growth rates, (2) vitamin B1 intake into the cell, (3) genetic profile of 27 different thiamine related genes and (4) the enzyme activity of several B1-dependent proteins.
They found that supplemental vitamin B1 stimulated more of an increase in growth in the mutated Huntington gene cells than the control cells, suggesting the Huntington cells had a higher requirement for vitamin B1. In addition, vitamin B1 intake, and therefore intracellular levels, was increased in the Huntington cells compared to control. Enzyme activity did not differ between cell types, but the expression of genes related to B1-dependent energy metabolism did differ between the control and mutated cell groups.
Vitamin B1 is known for its role in energy metabolism and deficiency has been linked to a several neurological syndromes such as Alzheimer’s disease and Wernicke encephalopathy, which suggests it may play a role in Huntington’s disease. Although this study was done in vitro (in test tubes), the increased expression of B1-related genes upon supplementation of B1 suggests intracellular vitamin B1 levels may play an important role in the manifestation of this enigmatic disease.
(Advances in Clinical and Experimental Medicine, August 2017)
Role of thiamine in Huntington's disease pathogenesis: In vitro studies.
Cellular health – whether referring to brain cells, bone cells, or fat cells – impacts the health of the entire body. Health issues may arise and manifest differently for each person depending on one’s unique biochemistry. Some common examples of these manifestations include excess weight, headaches, and dry skin, driven by poor cellular metabolism. Quite literally, health and wellness begin at the cellular level.
A paradigm shift in women’s healthcare is happening right now. You may have noticed that much of the focus in medicine today has shifted from disease to prevention; however, what we commonly think of as “preventive” medicine (mammograms, PAP smears) is actually pre-symptomatic screening for earlier disease detection and diagnosis. Prevention can be facilitated by the optimal nourishment of cells with micronutrients (vitamins, minerals, and antioxidants), as these fuel the cell and are involved in hundreds of metabolic reactions and physiological process. Some of these include detoxification, energy production, neurotransmitter balance, sleep quality, cognition, and immunity. Therefore, micronutrients profoundly affect mood, skin, hormone balance – every organ, endocrine, and body system is impacted. In fact, the nutrient-hormone connection is huge. Did you know that many female cancers – breast, uterine, ovarian – may occur when estrogen is metabolized into toxic by-products that are not eliminated? To keep estrogen metabolism in the body safe, women are encouraged to focus on these micronutrients:
- Magnesium activates the enzyme that removes toxic forms of estrogen.
- Vitamin B6 protects genes from estrogen-induced damage.
- Vitamin B3 increases adiponectin, a weight loss hormone.
- Vitamin A regulates leptin, a hormone that suppresses appetite.
- Cysteine prevents toxins in breast tissue from becoming cancerous.
These nutrients and dozens others behave like hormonal housekeepers, and lacking even one of these can set the stage for compromised health: vitamin deficiency can manifest as fairly benign conditions (lack of energy or poor sleep), or more serious illness (allowing the uncontrolled growth of cancerous cells to grow and invade healthy tissue).
Because we are all biochemically unique, micronutrient deficiencies may lead to different symptoms in different women. Find out yours, and take steps to correct them, by taking your micronutrient test today.
For more information on nutrients impacting estrogen levels, download our nutrient wheel!
Topics: Women's Health, estrogen and breast cancer, Chronic Fatigue, micronutrient status, Hormone Imbalance, Micronutrients and Estrogen Imbalance, Ovarian Cancer and Nutrition, Breast Cancer and Nutrition
Pharmaceutical medications help millions of Americans cope with clinical symptoms every day, but most are not without side effects. In fact, the side effects of a medication are often worse than the original condition according to many patients. One reason for this is that prescription drugs very often cause nutrient depletions, which manifest clinically in very significant ways. A classic example is coenzyme Q10 deficiency caused by statin medications. Statins block an enzyme that affects cholesterol production, but the same enzyme is needed to manufacture the important antioxidant coenzyme Q10, which is a key nutrient needed for cellular energy metabolism proper heart function. So if you block this enzyme (called HMG-CoA reductase for hydroxyl-3-methylglutaryl coenzyme A, which is why statins are known generically as HMG-CoA reductase inhbitors), you may lower cholesterol, but as a consequence you may cause a coenzyme Q10 deficiency, which can manifest as low energy and muscle pain.
Why is this so common? The reason is simple – the pharmaceutical approach is fundamentally different from the nutrient repletion approach in that medications alter or interrupt metabolic pathways to achieve a clinical result while nutrient repletion supports or helps maintain the optimal function of a metabolic pathway to achieve balance. In general, medications are palliative in that they focus often on the relief of symptoms. Conversely, nutrient repletion is curative and the goal is optimal cellular function of which a side effect is relief of symptoms.
This is not to say that medications have no place in health, but they do have a role in nutrient depletion which can cause the unpleasant and dangerous side effects. Especially in the age of polypharmacy – when people take more than one medication simultaneously (including over the counter meds) – nutrient depletions caused by drugs deserve a closer look. Here are some examples of how medications can deplete micronutrients:
- Meds can interrupt endogenous production of a nutrient (statins and CoQ10)
- Meds impairs absorption in the gastrointestinal tract (antacids and B12)
- Meds can create reactive oxygen species and thus “use up” antioxidants (NSAID and cysteine)
- Meds can increase urinary excretion of nutrients (diuretics and minerals)
- Meds can alter the gut microbiome (antibiotics and vitamin K)
- Meds can impairs mitochondrial function and cellular respiration
Adding to the problem is that fact research on drug-induced nutrient depletions is comparatively sparse compared to the giant funding allotted to pharmaceutical development and testing. In addition, there is a lag time between the market introduction of a blockbuster drug and potential nutrient depletion-induced side effect data. An example of this is research in the past decade that implicates antacids (proton-pump inhibitors) as a causative factor in cardiac events due to their tendency to deplete magnesium. The strong link between PPI use and arrhythmias (irregular heartbeat) may be caused by magnesium depletion, which may also explain an increased risk in bone fractures for people on long-term PPI use according to the FDA. Although research on PPI-induced magnesium deficiency emerged in the last few years, PPIs have been widely used in the market since 1990. In some cases, the research on drug-induced nutrient depletions may not emerge for many years after a drug is widely accepted into the market.
If you are taking a medication, have your micronutrient levels tested today.
Topics: statin, Intracellular Analysis, micronutrient deficiencies, Advanced Nutritional Testing, Effects of Statins on CoQ10, Drug-induced Nutrient Depletion, Functional Micronutrient Testing, Antacids, Functional Medicine
When people think of autism and nutrition, the first thing that often comes to mind is food sensitivities, especially given the widespread attention to the impact of certain additives and common triggers (such as wheat or dairy) on that condition.
Even more paramount, is the evidence suggesting that Autism is largely a whole-body disorder in which an individual's biochemistry affects the brain, learning and behavior. Restoring balance within the body through food and nutrients, therefore, becomes essential. The good news is, nutritional deficiencies that are impacting your child’s neurological development can be corrected. The list below includes specific micronutrients suggested to have a role in the development and treatment of autism:
Vitamin D: High-dose vitamin D therapy reversed autistic behaviors in severely deficient children; maternal vitamin D deficiency may predispose children to autism. A landmark trial further indicates that vitamin D supplementation helps children with ASD.
Vitamin A: One cause of autism may be a defect in a retinoid receptor protein (G-alpha protein) that is critical for language processing, attention, and sensory perception. Evidence suggests that natural vitamin A fixes this protein defect in autistics.
Folate: Oral folate therapy can resolve symptoms of autism in some cases, particularly in autistics with genes that impair folate-dependent enzymes.
Glutamine: Blood levels of this amino acid - which acts as a neurotransmitter - are particularly low in autistics. Glutamine also helps prevent leaky gut syndrome, which can exacerbate autistic symptoms.
Vitamin C: Improves symptom severity and sensory motor scores in autistic patients possibly due to interaction with dopamine synthesis; it also has a strong sparing effect on glutathione.
Glutathione & Cysteine: Both are commonly deficient in autistic patients. Low antioxidant status impairs detoxification and methylation processes, and has been linked to neurological symptoms in autism, which is often considered an oxidative stress disorder.
Vitamin B1: Deficiency linked to delayed language development; supplementation may benefit autistic patients.
Vitamin B12: Low B12 impairs methylation (detoxification), which can cause the neurological damage responsible for many autistic symptoms. B12 deficiency can cause optic neuropathy and vision loss in autistics; B12 raises cysteine and glutathione levels.
Vitamin B6: Cofactor for the neurotransmitters serotonin and dopamine; conversion of B6 to its active form is compromised in many autistics. Supplementation trials with B6 resulted in better eye contact, improved speech, and fewer self-stimulatory behavior in autistics. Some consider B6 in combination with magnesium to be a breakthrough treatment for autism.
Magnesium: Cofactor for the neurotransmitters that affect social reactions and emotion; autistics have low levels. Magnesium improves the effectiveness of B6 therapy.
Zinc: Eliminates mercury from brain tissue. The zinc/ copper ratio is particularly low in autistic kids, and low zinc impairs metallothionein, a protein that removes heavy metals from the body.
Carnitine: Transports fatty acids into cells. Low carnitine status, a common feature of autism, impairs the ability to use fatty acids for learning and social development.
The longer a child goes with Autism, the harder they are to reach. Evaluate your child's micronutrient status today!
For a copy of SpectraCell's Nutrition Correlation chart on autism, click here.
Topics: Cysteine, zinc, folate, Vitamin D, Carnitine, Magnesium, Vitamin C, Vitamin A, Vitamin B6, Vitamin B12, autism, Glutamine, Glutathione, Vitamin B1, nutrition and autism, nutrition speaks, autistic symptoms, micronutrient deficiencies, autism speaks, integrative approach to autism, alternative therapy for autism
We’ve all heard the proverbial advice for achieving a healthy body and maintaining our weight: exercise and “eat right.” But for those who really want to delve further into the science behind an enviable metabolism, we offer a list of vitamins with an explanation of their role in the body’s ability to burn fat and build muscle.
- Vitamin A: This vitamin is particularly good at regulating how genes are expressed. Although genes do determine to an extent how the body stores or burns fat, our genes are, simply stated, not our destiny. Two persons with the same gene may express it very differently, depending on their individual cellular environment. This is where vitamin A enters the picture. It can actually enhance the expression of certain genes that lower a person’s tendency to store food as fat. If one is vitamin A deficient, s/he may be pre-disposed to storing fat tissue. On the other hand, correcting a vitamin A deficiency may have a different, more positive effect, as studies have indicated that vitamin A may reduce the size of fat cells.
- Vitamin D: Similar to vitamin A, vitamin D (commonly referred to as the “sunshine vitamin”) affects genetic expression, including the way that fat cells develop. A vitamin D deficiency is strongly linked to poor carbohydrate metabolism: instead of efficiently burning carbohydrate for fuel (which consequently helps impart energy and mental focus), the body instead stores carbohydrate as fat. Correcting a vitamin D deficiency can boost metabolism by reversing this deleterious effect.
- Vitamin E: This micronutrient affects metabolism by inhibiting immature fat cells from developing into mature fat cells, which are more “stubborn,” metabolically speaking. The cumulative effect of this is a reduction in fat storage.
- Vitamin B3: Also called niacin, vitamin B3 can increase the hormone adiponectin, which is secreted by fat cells. Adiponectin’s main function is to signal cells to burn fuel. It also has a role in helping muscles use glucose for energy rather than storing it as fat.
- Vitamin B5: Some evidence suggests that vitamin B5 (AKA pantothenate or pantothenic acid) might be helpful for weight loss because it has been associated with less hunger when dieting. At the cellular level, vitamin B5 activates the enzyme lipoprotein lipase, which breaks down fat cells.
This list is by no means exhaustive: in fact, there are multiple micronutrient influences on weight loss. These micronutrients work both individually and synergistically, and repletion often promotes clinical benefits throughout the body. It should come as no surprise that micronutrient adequacy also supports heart health and energy levels. Therefore, discovering (then correcting) micronutrient deficiencies becomes a critical first step in improving overall health.
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Tired of not getting the results you want? Interested in learning how you can improve the efficacy of your weight management routine? Get tested and find out how your micronutrient status stacks up!
Topics: micronutrients, Vitamin D, Vitamin E, Vitamin A, Vitamin B5, Vitamin B3, Vitamins and weight loss, Role of micronutrients in weight management, Effective weight loss, Effective weight management, integrative approach to weight loss, micronutrients and weight loss