There are more health claims made about vitamin D than perhaps any other vitamin.  Media stories touting vitamin D for this ill or that are common, particularly in the age of COVID-19. We’re also frequently told Americans don’t get enough vitamin D, with surveys showing as many of 40% of individuals have below optimal amounts in the blood. So how do we get vitamin D and what claims are true and backed by research?  Let’s take a closer look at vitamin D to flesh out what we know for sure and where more research is needed. 

What is Vitamin D and How Do We Get It?

Molecularly, vitamin D is a group of fat-soluble compounds with a four ringed cholesterol backbone. What’s most important to know is that it comes in two forms — as vitamin D2 in food and as vitamin D3 in our skin.

Vitamin D3
Our skin is our primary source of vitamin D, but it begins there as an unorganized and inactive form, requiring UV exposure to convert to usable vitamin D3. Conversion via UV light is exceedingly efficient, and it’s estimated brief exposure of the arms and face is equivalent to ingesting 200 international units day. Conversion varies however with skin type (darker skin converts more), latitude, season and time of day. Infants, disabled persons and older adults often have inadequate sun exposure as well, and the skin of those older than 70 also does not convert vitamin D as effectively. Interestingly, vitamin D also requires temperature to be activated, so you may not get as much of a benefit from sunlight in the winter months as you might expect.  

Vitamin D2
Because it is fat-soluble, dietary vitamin D2 is best absorbed with fat in the diet and fish is a common source. Uptake can be negatively impacted by disorders associated with fat malabsorption such as celiac disease, Crohn’s disease, pancreatic insufficiency, cystic fibrosis, short gut syndrome and cholestatic liver disease.

Vitamin D in the Body: What We Know It Does

Once activated and in the bloodstream — either by UV exposure or absorption through the diet — the liver converts vitamin D to 25-hydroxyvitamin D (25[OH]D), and then the kidneys further convert it to 1,25 hydroxyvitamin D, the most active form of vitamin D in the body. For this reason, kidney and/or liver problems can also negatively impact vitamin D levels.

Interestingly, all cells in our bodies have receptors for vitamin D, and this has in part fueled the varying claims as to how it might impact health. What we know for certain is that it helps with calcium absorption in the gut, regulating calcium levels via the kidneys, and regulating parathyroid hormone. Vitamin D’s role in calcium regulation and absorption means it has a direct impact on healthy bone growth and turnover. For this reason, you often see it in calcium supplements.

Research has also shown a clear correlation between Vitamin D and muscle health, including research showing improved lower body strength. Some research has also shown vitamin D can help prevent falls in the elderly.

Notable Areas Where the Jury is Still Out

• Vitamin D has been thought to lower the risk of cancer, but currently, there is insufficient evidence to support this, though there are many ongoing studies.
• There is also insufficient evidence showing that vitamin D helps improve autoimmune conditions and respiratory conditions such as asthma, COPD and acute viral respiratory diseases.  In a large study from the UK, no association was found between vitamin D levels and risk of mortality from COVID-19.
• Although low vitamin D levels have been associated with an increased risk of cardiovascular disease in some studies, there is no evidence that vitamin D supplementation improves cardiovascular outcomes.
• Similarly, a growing number of trials examining the effects of vitamin D supplementation on pregnancy and birth outcomes show conflicting results, with some showing reduction in risk of low birth weight, but more data is needed.

Naomi L. Albertson M.D. is Board Certified by the American Academy of Family Physicians and specializes in the non-surgical management of musculoskeletal problems, sports injuries, concussions, and the treatment of osteopenia and osteoporosis.

Mounting evidence suggests that we may be able to live a longer, healthier life by strategically restricting our energy intake. For many years the scientific community has known that a surplus of energy intake results in the storage of fat, which is linked to chronic disease, and premature death. However, now emerging evidence suggests that restricting calories may be able to slow the rate in which we age. Aging can be categorized as either primary or secondary. Primary aging is considered inevitable at the date of this publishing and is the biological maturing and eventual breakdown that accompanies the years of age beyond 30.  Secondary aging comes from external influences such as obesity and lifestyle factors that cause cellular damage and is not part of the natural aging process. (2)

What is calorie restriction? Calorie restriction describes a process where one limits the amount of food they consume. The term calorie is a shortened term originating from kilocalorie and is used as a measurement of food energy. When the body has an excess of calories beyond what it needs to function it stores those calories in our body as fat. Despite the diet industry’s most sincere efforts and propaganda, studies still do not support the effectiveness of one fad diet over another for weight loss. (13) This means, weight gain, and weight loss are ultimately determined by the number of calories consumed, and the number of calories expended.

Earlier we identified obesity as contributing to secondary aging. The scientific community has established that being overweight, or obese dramatically increases your risk of cancer, heart disease, and type II diabetes, among other chronic disease, thereby reducing life expectancy. In fact, people that are 100 pounds or more overweight can expect a life expectancy that is nearly 14 years less than the national average. This is a shorter life expectancy than that of someone who is of a healthy weight and smokes cigarettes. (3, 12) A calorie reduction below what your body is expending results in weight loss, and for those who have a higher than healthy level of body fat, can expect a reduction in not just their weight but in secondary and primary aging.

There are many misconceptions of what constitutes being overweight or obese.  A person is classified as being overweight if they have a BMI (body mass index) of 25 or higher, and obese if they have a BMI of 30 or higher. BMI is calculated by dividing your weight in kilograms by your squared height in meters. BMI is likely a fair indicator if you are relatively inactive. If you are engaged in a fitness program or are an athlete, an alternative approach to determining healthy weight is by determining percentage of body fat. A healthy body fat is typically considered to be between 8-22% for men and 20-35% for women (aged 18-34).  A classification of obese may be assigned if someone has a body fat percentage of 26% or higher for men and a body fat of 39% or higher for women. (7) As always if you’re not sure where you fit into these metrics see a credentialed fitness professional or consult with your primary care provider.

It is estimated a calorie deficit of 200-500 calories daily is required to achieve healthy weight loss. Two ways to achieve this deficit are to reduce calorie consumption and increase calorie burn (expenditure). Calorie burn can be increased through additional physical activity; however, it should be cautioned that one can consume calories at a far faster rate than physical activity can burn them. As an example, it is estimated that a 180-pound man burns approximately 14 calories per minute jogging (1). As a point of reference, a single Hershey kiss contains 22 calories.  The lesson here is to use physical activity in addition to a nutritious diet, not in place of a nutritious diet.  (For more information on a nutritious diet visit choosemyplate.gov.) Give special attention to the section on vegetables, especially non-starchy vegetables as they are high in vitamins and minerals and low in calories.

For persons of a healthy weight, calorie restriction appears to offer slowed primary aging. The current school of thought is that primary aging is slowed as a result of a protective cellular reaction triggered by the calorie restriction. There is still much we do not know about the mechanisms responsible for this anti-aging phenomenon and some debate among scientists exists. However, the most common consensus among scientists is that this reaction collectively comes from activating sirtuins, increasing AMPK, impacting MTOR, and an improvement in blood sugar. (8,10,15,16,17,18) If you do not know what any of that means here’s a quick break down but don’t fret if you are not familiar with the lingo.

• Sirtuins are responsible for DNA expression and control acetyl groups, as well as activate the mitochondrial antioxidant function. (8,16,17) Oxidative damage is believed to play a role in primary aging. Acetyl groups are important because they control the energy that proteins use during cell replication.
• AMPK (Adenosine Monophosphate Protein-activated Kinase) detects the presence of nutrients or prolonged absence of nutrients, which then triggers the fragmentation/breakdown of damaged mitochondrial components (mitochondria are the powerhouse of the cell) that need to be rebuilt, increasing mitochondrial health and efficiency. (4,16,17)
• MTOR (mammalian target of rapamycin), specifically TORC1 regulates protein building and cell growth. It is theorized a reduction in TORC1 and in turn a reduction of cellular division results in reduced DNA damage, and less inflammation. (11,17)
• In terms of handling blood sugar, there are two important molecules at work. These proteins are Thioredoxin-interacting protein (TXNIP), and Thioredoxin-1. When TXNIP is stimulated by insulin (which results when we eat) cell stress resistance is reduced resulting in increased oxidative damage to DNA. It is theorized that during calorie restriction, Thioredoxin-1 increases which increases oxidative stress resistance, increases nonoxidative glucose disposal, and increases insulin sensitivity (improves use of insulin and absorption of sugar) as well as reduces damage to DNA (and thus slowed DNA aging) (10,15).

Regardless of how precisely these mechanisms work or interact what we currently believe and have pieced together is a reduction in calories likely:

• Triggers a protective response in the body that helps:
  • Protect mitochondria from free radical damage (mitochondria are the energy makers of the cells)
  • Increases cell sensitivity to insulin and in turn increases absorption of blood sugar into the muscle
  • Induces cellular stress resistance and cell cleansing, which shuts off cell replication. Think of cell replication like a copy machine, if you do not use the original for each copy, but instead use a copy to make a copy, each time the copy gets blurrier. This is thought to also occur in our cells, therefore the less copies we make or the slower we make them the slower the aging process occurs.
• Appears to reduce risk of age-related diseases such as heart disease, cancer, and diabetes.
• Begins at 10%-40% reduction in calories per day (from normal)
• Starvation is too far! You still need to get the vitamins, minerals, and nutrients required to aid your body in recovery, and immune function otherwise your efforts will be counterproductive, which can be done by increasing your consumption of non-starchy vegetables.
• Calorie restriction can be accomplished by all types of fasting schemes. For example, fasting can take place daily for 12-16 hours, every other day, or over the weekends only. The important thing is achieving that 10%-40% reduction while still getting the proper nutrition necessary. (5)

The takeaway here is achieving and maintaining a healthy weight is the first step to a healthy lifespan and the incorporation of strategically fasting, may bring additional health and longevity. Fasting has been embedded in our culture in many ways from traditional religious observances as well in the fitness industry, but the question is what scheme and plan will work best for you. Most would agree it’s the health span (length of superior quality of life attributed to good health) more than the lifespan that’s important, and while there is currently no fountain of youth this appears to be a good place to start.

Remember, of course, to consult with your primary care provider before undergoing dietary changes.

Jeremy Kring holds a Master’s degree in Exercise Science from the California University of Pennsylvania and a Bachelor’s degree from Duquesne University. He is a college instructor where he teaches the science of exercise and personal training. He is a certified and practicing personal/fitness trainer, and got his start in the field of fitness training in the United States Marine Corps in 1998. You can visit his website at jumping-jacs.com

References

• American Council on Exercise. (2009). Retrieved from https://acewebcontent.azureedge.net/assets/education-resources/lifestyle/fitfacts/pdfs/fitfacts/itemid_2666.pdf
• Anstey, K., Stankov, L., & Lord, S. (1993). Primary aging, secondary aging, and intelligence. Psychology and Aging, 8(4), 562–570. doi: 10.1037//0882-7974.8.4.562
• Tobacco-Related Mortality. (2018, January 17). Retrieved from https://www.cdc.gov/tobacco/data_statistics/fact_sheets/health_effects/tobacco_related_mortality/index.htm.
• Cantó, C., & Auwerx, J. (2011). Calorie Restriction: Is AMPK a Key Sensor and Effector?Physiology, 26(4), 214–224. doi: 10.1152/physiol.00010.2011
• Derous, D., Mitchell, S. E., Wang, L., Green, C. L., Wang, Y., Chen, L., … Speakman, J. R. (2017). The effects of graded levels of calorie restriction: XI. Evaluation of the main hypotheses underpinning the life extension effects of CR using the hepatic transcriptome. Aging, 9(7), 1770–1824. doi:10.18632/aging.101269
• Hadad, N., Unnikrishnan, A., Jackson, J. A., Masser, D. R., Otalora, L., Stanford, D. R., … Freeman, W. M. (2018). Caloric restriction mitigates age-associated hippocampal differential CG and non-CG methylation. Neurobiology of aging, 67, 53–66. doi:10.1016/j.neurobiolaging.2018.03.009
• Howley, Edward T., and Dixie L. Thompson. Fitness Professionals Handbook. Human Kinetics, 2017.
• Imai, S. I., & Guarente, L. (2016). It takes two to tango: NAD⁺and sirtuins in aging/longevity control. NPJ aging and mechanisms of disease, 2, 16017. doi:10.1038/npjamd.2016.17
• Jacobs, Patrick L. NSCAs Essentials of Training Special Populations. Human Kinetics, 2018.
• Johnson, M. L., Distelmaier, K., Lanza, I. R., Irving, B. A., Robinson, M. M., Konopka, A. R., … Nair, K. S. (2016). Mechanism by Which Caloric Restriction Improves Insulin Sensitivity in Sedentary Obese Adults. Diabetes, 65(1), 74–84. doi:10.2337/db15-0675
• Jossé, L., Xie, J., Proud, C. G., & Smales, C. M. (2016). mTORC1 signalling and eIF4E/4E-BP1 translation initiation factor stoichiometry influence recombinant protein productivity from GS-CHOK1 cells. Biochemical Journal, 473(24), 4651–4664. doi: 10.1042/bcj20160845
• Kitahara CM, et al. Association between Class III Obesity (BMI of 40–59 kg/m) and Mortality: A Pooled Analysis of 20 Prospective Studies. PLOS Medicine. July 8, 2014. DOI: 10.1371/journal.pmed.1001673.
• Kuchkuntla, A.R., Limketkai, B., Nanda, S. et al. (2018). Fad Diets Hype or Hope?. Current Nutrition Reports 7: 310. doi.org/10.1007/s13668-018-0242-1
• Mitchell, S. E., Delville, C., Konstantopedos, P., Hurst, J., Derous, D., Green, C., … Speakman, J. R. (2015). The effects of graded levels of calorie restriction: II. Impact of short term calorie and protein restriction on circulating hormone levels, glucose homeostasis and oxidative stress in male C57BL/6 mice. Oncotarget, 6(27). doi: 10.18632/oncotarget.4003
• Oberacker, T., Bajorat, J., Ziola, S., Schroeder, A., Röth, D., Kastl, L., … Krammer, P. H. (2018). Enhanced expression of thioredoxin-interacting-protein regulates oxidative DNA damage and aging. FEBS letters, 592(13), 2297–2307. doi:10.1002/1873-3468.13156
• Picca, A., Pesce, V., & Lezza, A. (2017). Does eating less make you live longer and better? An update on calorie restriction. Clinical interventions in aging, 12, 1887–1902. doi:10.2147/CIA.S126458

(-) “When and+ accumulates, such as during scarcity of nutrients especially glucose, sirtuins are activated….”

• Son, D. H., Park, W. J., & Lee, Y. J. (2019). Recent Advances in Anti-Aging Medicine. Korean journal of family medicine, 40(5), 289–296. doi:10.4082/kjfm.19.0087
• Speakman, J.R. & Mitchell, S.E. (2011) Calorie Restriction. Molecular Aspects of Medicine, Jun:32(3):159-221. doi: 10.1016/j.mam2011.07.001