Sunday 29 September 2013

Menstrual Cycle Impact on Training and Performance

I know I'll be getting a lot of grief from male athletes for this one. After all, as if we're not getting chicked often enough in races!...

Don't shoot the messenger!!

Highlights

- How your menstrual cycle impacts your training and performance
- How to time your races against your menstrual cycle for peak performance
- How training can impact the frequency and duration of your cycle
- How severe calorie deficiency can lead to stress fractures
- How contraception pills can help you train better and strengthen your bones
- My recommendations on how to train to be ready to race at all times

Biology 101

As most of you already know, there are 2 "primary" hormones that differentiate men from women: Estrogen and Progesterone.

Estrogen
What many people don't know, is that Estrogen, in addition to controlling the development of sexual characteristics and development related to pregnancy, also plays important roles in bone protection, blood coagulation, menstrual cycle functioning, cholesterol production, and salt and water retention

In fact, the concentration of circulating Estrogen in the blood is the single most important determinant of bone mineral density in women.

Estrogen deficiency caused by Amenorrhea (missed period as a negative consequence of large training volume) is the most significant risk factor for osteoporosis (bone fragility) and stress fractures among active women). 

ATHLETE IMPLICATIONS: Estrogen also influences pulmonary function, body temperature, fat metabolism and blood plasma volume (therefore fluid retention and hydration), all critical aspects for endurance sports.

We're going to delve into the impact of Estrogen on training and performance later...

Progesterone

Progesterone is one of the primary hormones involved in preparing the female body for the conception of a newborn. It has multiple functions both in terms of preparing vital organs for the fertilization of the egg as well as gestation.

However, in addition to these important functions, Progesterone has been shown to be involved in a number of other physiological functions. 

Progesterone:

- Acts as anti-inflammatory and helps with immune response
- Regulates gall bladder activity
- Normalizes blood clotting, circulating zinc and copper levels, cell oxygen levels
- Increases the usage of fatty acids (fat) as a source of energy, raises glycogen stores and reduces lactate - all have obvious implications for athletes which I discuss further below
- Plays an important role in the signaling of insulin release and pancreatic function, thereby impact risk of developing diabetes

Your Menstrual Cycle and how it affects your training and performance

Let's start with the basics:

The menstrual cycle is typically 28 days long and is divided in half by ovulation on day 14:
- The first half of the cycle is called the Follicular Phase
- The second half is called the Luteal Phase.


ATHLETE IMPLICATIONS: Each of these phases has hormonal and physiological characteristics which have a significant impact on your training and performance, as I explain further down.


The Follicular Phase starts with menses (period) - following menses, Estrogen rises, peaking around day 14, right before ovulation. A burst of Estrogen at the end of the phase causes a surge in luteinizing hormone to initiate ovulation. Progesterone stays low

The Luteal Phase starts at ovulation - Progesterone rises, Estrogen drops and rises again towards the middle. The increase in Progesterone causes an increase in body temperature (to prepare for egg fertilization). If fertilization does not occur, both Estrogen and Progesterone drop quickly, triggering the onset of menses.



Source: www.sciencebasedmedicine.org/


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A note on bloating and PMS:

Why do you sometimes feel bloated during your cycle: high concentration of Progesterone during the Luteal Phase (phase 2) affects fluid balance, causing you to lose water and electrolytes. The rapid drop in Progesterone at the end of the phase (if egg is not fertilized) results in excess premenstrual water and electrolyte retention, creating that bloated feeling.

What causes PMS and what can you do about it: PMS is a series of uncomfortable symptoms triggered by the rapid drop of both Estrogen and Progesterone at the end of the Luteal Phase when the egg is not fertilized. 

The cramping during PMS is thought to be caused by the hormone prostaglandin, which is produced by the uterus and causes it to contract (the cramping). Birth control pills and anti-inflammatory drugs (such as Ibuprofen) can reduce cramps by inhibiting prostaglandin


A note on Ibuprofen and other over the counter anti-inflammatories: as I mentioned earlier, these drugs inhibit prostaglandin. But you have to be aware that prostaglandin plays a big part in the health of your gut lining, and inhibiting prostaglandin puts people at risk of deterioration in gut health and creates the potential for gut leakage (and it doesn't take long for that to happen).

Only limited research has been conducted on the effects of exercise on PMS (assign blame as you wish) - but whatever research was done did yield significant results supporting the theory that exercise does reduce PMS symptoms (results varied among individuals).
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So the impact on performance then?!

Well as I alluded to earlier, the Estrogen/Progesterone cycle influences:
1- Basal Body Temperature
2- Metabolism (utilization of fat vs. glycogen as fuel)

1- Impact on body temperature and its effects on training and performance

The chart below illustrates the change in your "Basal Body Temp" during the cycle. Basically, your Basal Body Temp is the temperature your brain considers to be "normal" and does not trigger either sweating to bring it down or shivering (for e.g.) to raise it.

As you can see from the chart, your Basal Body Temp rises gradually during days 14 to 24 (Luteal Phase), with a sharp "spike" around day 25.






Remember the hormonal chart above? This coincides with the gradual rise followed by a "spike" in Progesterone during that same period of time.

In effect, what is happening is that Progesterone is triggering an increase in your Basal Body Temp in preparation for the possible fertilization of an egg.

So on days 6-14 for example, a body temp below 36.2C is considered "normal", while on days 20-28, a body temp of 36.6C or higher is considered "normal". The difference may only be 0.4C, but that has big implications!

ATHLETE IMPLICATIONS:

The Hypothalamus in your brain acts as your "thermostat", regulating body temperature. When it detects a sudden rise in body temperature above your Basal Body Temp, it triggers sweating to cool you down and bring the body temp back to Basal.

What causes this to get triggered? It could be ambient temperature (walking in hot weather), exercise (active muscles producing heat as a bi-product), etc.

Now your muscles need that stable body temperature to continue functioning. I won't get into the chemistry of why that happens, but many have experienced how heat impacts ability to exercise. 

AND, your muscles don't really care that your Basal Body Temp is being adjusted upwards in preparation for the fertilization of an egg. They want the temperature to be "stable goddammit !!! What's all that about letting it rise to 36.6C or 37C ??!".

But here's the problem:

Days 1-14: Basal Body Temp is low - if body temp goes above it, that triggers sweating and cools it back down. Muscles are happy.

Days 14 onwards: Basal Body Temp is now high - sweating doesn't happen until body temp rises above the new, "now higher", Basal Body Temp. Muscles are NOT happy!

And muscles not happy = feeling horrible during training and lower performances = heat exhaustion...

And it's not just muscles: when exercising in heat, increased thermal strain comes with greater cardiorespiratory strain:
1. Sweating causes loss in blood plasma volume
2. Which causes a lower stroke volume (how much blood the heart pumps with each "beat")
3. Which leads to less oxygen to muscles
4. Which means that the heart has to beat faster to compensate
==> this is what we call cardiac drift: your HR rises by 3 to 5 bpm for every 1% body weight lost from dehydration

Of course, this can be averted with proper hydration - and now you can see why I'm always banging the table about hydration :-)

And who's the culprit behind all this: well it's Progesterone, because it is the one telling the Hypothalamus: "hey buddy, I'm preparing for egg fertilization, so don't you dare trigger sweating until the body temp reaches this new higher number!"

And here's another interesting piece of info: both Estrogen and Progesterone affect women's breathing during exercise. In fact, Progesterone has been shown to increase breathing and severity of asthma symptoms as well as the "Rate of Pereceived Exertion" or RPE (how much effort you "feel" you're putting out).

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A couple of side notes on this whole Basal Body Temp thing:

Head Adaptation: by training sporadically in moderate heat, your body becomes more efficient at sweating. In other words, it teaches your body to start sweating earlier at ALL body temperatures. This is one way to deal with this issue if you must train or race during those peak Basal Body Temp days.

Oh and by the way, as some of you may know, the reason your doctor has you monitor your body temp if you're trying to get pregnant is exactly because of this whole mechanism: a rapidly rising Basal Body Temp means that Progesterone is rising and ovulation is about to happen - perfect timing to conceive a future athlete!
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2- Impact on metabolism

Let's start with some general information which I'm sure female readers will love and male readers will hate.

Ok let me put it out there once and for all: women are better equipped for endurance racing than men "metabolically". Again, don't beat me up for it boys! Women have a better fat metabolism period.

In fact, if you were to look at average finishing times in running races between men and women, you will see the difference shrinking as the distance increases.


As a matter of fact, in 2002 and 2003, Pam Reed won the 217km Badwater ultramarathon, posting the fastest time overall, beating all the men.

If you would like to know more about this inspiring athlete, read her book: The Extra Mile.






You want further proof? Here are the differences between men and women for the world record over increasing distances:

- 5,000m: 11.0%
- 10,000m: 10.8% 
- Marathon: 8.5%
- 100km: 5.5%

Spot the trend there?

Studies have shown that women rely more on fat as fuel then men. A number of studies have shown that female athletes on average use 75% more fat than male athletes at efforts between 65% and 70% of VO2max (aerobic efforts).

Additional training further increases the number of mitochondria (cellular power plants) in muscles, thereby assisting in fat utilization (in both men and women). This type of training has to be specific to fat adaptation tough.

Of course, there's a catch: as you burn more fat, you burn less glycogen (the carbohydrate stores in your liver and muscles). And that's a good thing! Because while women are better at burning fat than men, they have lower glycogen stores to begin with.

Again, diet and training influences how much glycogen you can store, but still, no amount of training and diet can bring women's carb-storing capacity in line with men's.


So forget carbo-loading at races ladies! It doesn't do much! But still come along, we enjoy your company ;-)

In fact, relying heavily on carbs in your diet will teach your body to burn more carbs, but since you have a lower ability to store carbs in the first place, you could be leaving your naturally given fat-burning potential on the table!

And because of the higher fat utilization / lower glycogen utilization in women, the rate of muscle breakdown is lower, and you can recover quicker from workouts... (fantastic, just what we male athletes needed)

So what does all this have to do with the Menstrual Cycle?

Estrogen is partly responsible for higher fat utilization as fuel in women - when male rats are given Estrogen, they utilize less glycogen and have higher circulating fatty acids (indicating an increase reliance on fat as fuel). In fact, those same studies have shown that injecting these male rats with Estrogen increased their endurance.

Lance probably knows better, but wouldn't Estrogen be cheaper than EPO?








So this means that any heavy-training-induced drop in Estrogen level will affect your fat metabolism.

But it's not that clear-cut I'm afraid: Female athletes have shown an even higher level of fat utilization and lower lactate during the Luteal Phase, when Progesterone is high. 

So it seems that while Estrogen does provide women with a better fat metabolism then men, Progesterone is what maximizes that ability.


ATHLETE IMPLICATIONS:

That creates a bit of a dilemma right? We have 2 conflicting pieces of information now:

- Race during the Follicular Phase (phase 1) because low Progesterone keeps your Basal Body Temp low, ideal for your muscles to function well

- Fat metabolism peaks during the Luteal Phase (phase 2) when Progesterone is high.

What to do then?

While no significant studies have been conducted to explore these 2 conflicting phenomena, observations have shown that the best performances were reported during the early days of the Follicular Phase, and the worst during the Luteal Phase

In other words, expect to perform well when Estrogen is dominant and worse when Progesterone is dominant.

It seems that your body's temperature is more critical to your performance in endurance races than the "marginal" increase in fat utilization induced by Progesterone.

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So my personal take on how to structure training would be as follows:

- Improve your overall fat-adaptation so you can burn more fat in both phases
- Make sure you add some heat acclimatization into your training to "teach your body to start sweating earlier at all Basal Body Temps"
- Make sure you include higher-intensity training to develop glycogen storage capacity

==> This should equip you optimize your body to deal with any condition:

- If race falls during the Follicular Phase (phase 1): your Basal Body Temp is low (optimal), your fat metabolism has been increased through training, and while you do use a little glycogen, you have more of it since you trained to increase its storage capacity.

- If your race falls during the Luteal Phase (phase 2): your heat adaptation allows you to start sweating earlier despite the higher Basal Body Temp, the high Progesterone levels will make you more fat-efficient anyway, and you can tap into those glycogen stores to put the hammer down in the last few Kms!

General Note: in my opinion, specificity in training is key not just to get fitter and faster but also to stay healthy, injury-free, save time and avoid burnout. 
A training program with good specificity will capture the adaptations needed to work "around" your menstrual cycle and enable good performance throughout the month.
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How does heavy training affect the cycle and what can you do to fix it?

What does heavy training do to the cycle and your overall well-being

As we discussed at the beginning, low levels of Estrogen caused by excessive training without adequate caloric intake significantly increase risks to bone density.

Bone Mineral Density peaks for both sexes around age 30, but the "female peak" is lower than the "male peak". This means that female athletes need to be a lot more careful with how much pressure they put on their bones (e.g. increases in run volume). 

This becomes even more critical if irregularities in the menstrual cycle are observed (risk of low Estrogen), and this why your doctor would be asking you to take Vitamin D and Calcium supplements (importance of Vitamin D in bone health was discussed in a previous blog here).

Furthermore, heavy training shortens the Luteal Phase (phase 2), followed by cycles without ovulation and finally cessation of menses (amenorrhea), related to constantly low levels of Estrogen and Progesterone, where levels of Estrogen would be similar to post-menopausal women.

And once again, Estrogen is that gives women the metabolic "edge" through higher fat utilization. Lower Estrogen starts to give that advantage away. Combine that with lower glycogen storage capacity, and you can guess the impact on training and racing.

So what can you do?

Research has shown that this hormonal imbalance is not because of the stress of exercise but rather because of severe caloric deficit
Some studies have shown that women who exercise heavily but fuel well (pre, during, post) prevent amenorrhea.


One way to help increase bone density in active women with menstrual irregularities: oral contraceptives, which increase Estrogen and regulate the cycle.

However be careful, different pills have different concentrations of Estrogen / Progesterone, and some of them "cycle" the ratio 2-3 times during each menstrual cycle.



One additional word of caution: 
check iron levels if heavy bleeding occurs regularly during menses.

A special thanks to Dr. Jason Karp whose book Running for Women was an important source of information for this article.

Happy training!

T

Saturday 21 September 2013

1 billion people on our planet are deficient in Vitamin D


Is that even possible? Being the geeky person I am, and even though I’ve been hearing about Vitamin D deficiency for years, I was still quite skeptical about this, so I dug a little: it turns out that there is plenty of evidence to support this claim!

Not 1, not 10, but dozens of studies over the past decades indicate that us Homo Sapiens have been becoming more and more deficient in Vitamin D over the past decades, with deficiencies currently at there peak.

But still, I was skeptical, and asked myself a few questions and set out trying to answer them:

  • Who actually determines the level below which we are “deficient”?
  • So what if we are deficient? We would see a lot of sick people if it is true that 1 billion people are deficient and if that deficiency presents hazards to our health and well-being.
  •  What changed? Were human beings always deficient or is it a new phenomenon caused by our “way of life” in the 20th and 21st century?
  • What are the symptoms of deficiency? What are the risks?
  • And what can we do to remedy the situation?




Before I get started, a small disclaimer: while I did major in Biology and Physiology as a pre-med in college (BS in Biology), I am NOT a medical professional and my opinions are based purely on my education, my avid interest in all things health, medical and fitness related, and my ongoing studies in physiology and nutrition. Please do NOT take my writings as medical advice and seek a qualified medical practitioner for sound medical guidance.

Throughout this blog, you will see some paragraphs written in Italic. These indicate a “nerd alert!!!!” where I dig a little deeper into certain aspects. Those paragraphs can be skipped entirely without losing much to be honest!



Ok, here we go:

So what is Vitamin D and why should you care about it?

You see there are 2 types of vitamins: water soluble ones (such as Vitamins B and C) and fat soluble ones (such as Vitamin D, A, E and K).

Another major difference between them is that most of the Vitamin D that you need can actually be manufactured (technically synthesized) by your body. In fact, if you were to rely purely on ingested vitamin D (from foods or supplements), you’d pretty much have to eat oily fish and pop dozens of pills daily, not fun, sustainable, or healthy.

For the sake of simplicity, I’ll use the term VitD to refer to Vitamin D as well as its active and inactive derivatives and precursors.

Funny enough, VitD is not classified by the FDS as an “essential dietary vitamin”. The reason for that is NOT because it is not essential, but because the classification takes into account the fact the it can be synthesized by the body on its own.

Of course if the body is not capable of doing that adequately (due to limited sun exposure for example), then we’re in trouble and we have to get it from somewhere else.

We’ll come back to how your body manufactures this vitamin, but let’s talk a bit more about what it is and what it does first:

VitD is essentially a steroid hormone. Well technically, it’s a secosteroid, which is a molecule similar to a steroid molecule except that 2 of the carbon atom rings are “broken”.

The term Vitamin D generally refers to numerous forms of this steroid, but 2 forms are the most important for human being: ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3). Vitamin D2 is synthesized by plants. Vitamin D3 is synthesized by humans in the skin when it is exposed to sunlight.

Most of the active forms of VitD in the body are derived from Vitamin D3.


So what’s the big deal about VitD?

Hundreds of studies have been done on the functions of VitD and what we know is staggering:
  • VitD regulates over 1000 different genes in the human body!
  • Almost every cell in the human body has a VitD receptor! (not shocking given that VitD is a hormone and most cells have hormone receptors, but still…
  • VitD is critical for bone health (density and mineralization):
VitD is a primary regulator of calcium (C) and phosphate (PO4) homeostatis; it regulates the absorption of Ca and PO4 in the intestinal tract and consequently its availability in the blood stream and to muscles and bones. It also indirectly regulates the rate of resorption in bone as well as the parathyroid hormone. Note that it is not the only regulator, but a primary one – other factors come into play.

Please contact me for additional readings on calcium sufficiency and supplementation.

  • Low levels of VitD have been associated with increased mortality
  • Numerous studies support the hypothesis that VitD deficiency is linked to a number of diseases, including cardiovascular, neuromuscular, metabolic, digestive, and others (more on that later)
  • Studies have shown that athletes and active people are at a higher risk of VitD deficiency than others – and many of the early symptoms of VitD deficiency (e.g. lethargy, muscle weakness) are incorrectly attributed to low iron levels – please see section below on VitD and Athletes




Below is a table in which I summarize the diseases and disorders linked to VitD deficiency:

DISEASES & DISORDERS RELATED TO VITAMIN D DEFICIENCY
Name of Disease
Disease Details
Scientific Evidence
Familial hypophosphatemia
Bone deformation in children caused by low phosphate levels
Strong
Fanconi syndrome hypophosphatemia
Kidney disease
Strong
Hyperparathyroidism
Overactive parathyroid glands regulating Calcium and Phosphate
Strong
Osteomalacia
Softening of bone and muscle weakness in adults
Strong
Psoriasis
Severe skin disorder
Strong
Rickets
Weakness and deformity in bones among children
Strong
Falls in Elderly
Evidence of VitD reducing incidence of falls among elderly
Good
Muscle weakness/pain
Evidence of VitD reducing muscle weakness among adults & children
Good
Osteoporosis
Reduced bone density and fragility in adults
Good
Asthma
VitD observed to reduce symptoms
Observed
Autoimmune diseases
VitD found to have anti-inflammatory and immunomodulating effects
Observed
Cancer prevention
Studies indicate inverse association btw VitD and colorectal, cervical, breast, and prostate cancers
Observed
Cardiovascular disease
Observed relationship with increased CVD occurences
Observed
Cognition
Better cognitive test results among elderly with VitD supplementation
Observed
Hypertension
Observed: low VitD levels linked to higher blood pressure
Observed
Mood Disorders
Low VitD linked to depression and PMS
Observed
Multiple sclerosis
Lower MS rates in greater sunlight and higher consumption of vitD rich fish
Observed
Type 2 diabetes
VitD shown to improve insulin sensitivity
Observed
Source: www.mayoclinic.com


So what level is considered “Deficient”

Well unfortunately, that’s not very clear. While dozens of studies have been done and conclusions have been reached that lower levels of circulating VitD can lead to numerous problems as listed above, there is no consensus on a threshold or range.

There are however some general guidelines put forward by a number of credible sources. Here is what is considered “sufficient”:

  • The Vitamin D Council: 40-80ng/ml (based on over 1,000 studies reviewed)
  • The US Endocrine Society: 30-100ng/ml
  • The Food and Nutrition Board: >20ng/ml
  • General laboratories: 40-100ng/ml
  • Australian Family Physician journal: >40ng/ml

According to the Archives of Internal Medicine, over 70% of Americans have been found to have levels of circulating VitD below 30ng/ml, classifying them as deficient. (this study was published in 2009 and based on samples take between 2001 and 2004, but there are no indications that levels have recovered during the past 10 years).

(At the end of this blog, you will find a couple of additional examples of studies showing the correlation of low levels of VitD with certain disorders).


So did we like “wake up one day and realize we’re deficient”??


Well, not really.

Of course it’s hard to tell whether people before the 20th century were deficient, but the data available to us suggests that we’ve been becoming increasingly deficient since the 1950s, decade after decade.


It’s hard to correlate that to specific phenomena, but obviously the human race went through a revolution of some sorts after World War II with a big acceleration in urbanization and industrialization. 



Here are some of the trends which could have contributed to increased deficiency in VitD:

  • We collectively spend a lot less time outdoors
  • The “scare” around skin cancer has caused an explosion in sun-screen products
  • Our average “work week” has increased (in terms of number of hours)
  • The frequency and duration of “vacations” have dropped
  • The general nutrient-density of our diet has deteriorated (quality of foods we consume)
  • Metabolic (obesity, diabetes) and digestive disorders are on the rise, increasing the demand for vitamins and minerals in our bodies




Ok, but that’s for the general population, what about us “athletes”?







Well there are 2 things to be considered here:
  1. Are athletes generally more or less likely to be deficient?
  2. Does VitD deficiency (and supplementation) impact performance?
Regarding question 1:
  • Willis et al found in 2008 that 77% of German gymnasts had VitD levels below 35 ng/ml and 37% had levels below 10 ng/ml (clearly deficient)
  • In study published in 2006 by the International Journal of Sports Medicine, the average VitD levels for cyclists in France was found to be 32ng/ml. This is surprising for a sport with so much sun exposure!

In my personal opinion, the increased metabolic and mineral demands in athletes justify an even higher threshold of minimum circulating levels of VitD.

I mean think about it: our bones are stressed, our muscles are stressed, we lose calcium and other minerals through sweating and metabolic needs and repair, and we are in a constant state of “inflammation”.

All of these factors justify the need for a higher minimum level of VitD than the average population to ensure proper calcium and phosphate absorption, bone density and mineralization, optimal digesting and endocrine function and reduced inflammation!

Regarding question 2 (performance):
An article published in May 2009 of the Journal of Medicine and Science in Sports and Exercise highlights observations from numerous studies:

  • Positive relationship between UV-induced Vitamin D and athletic performance
  • Physical and athletic performance is seasonal: peaking during high-UV periods and declines when UV-exposure declines
  • VitD increases size and number of fast twitch fibers in muscles
  • Improvement in athletic performance observed when levels go above 50ng/mL
  • Longer recovery needed between workouts for athletes with lower VitD levels

There are also some seen but yet untested observations that low levels of VitD impact VO2max, so there you go! Who wants that!?

There are also some observations where VitD supplementation has been seen to reduce inflammation (faster recovery) due to lower cytokines and better production of anti-inflammatory cytokines. Again without getting too geeky, citokines are a group of hormone-like proteins and glycoproteins whose function is to regulate the body’s response to inflammation, infection, and other disorders.

BUT and it’s a big BUT: studies have shown that these positive effects only impact people who are deficient in VitD, and that “extra” supplementation in VitD if you are not deficient does NOT enhance performance (sorry to disappoint) - here that Lance?.


So how does our body manufacture VitD anyway?

According to the Journal of Nutrition (2003), between 10,000-20,000 International Units (IU) of VitD can be synthesized by human skin from 30min of UV exposure (sunlight).  

In fact, our skin uses a derivative of the existing cholesterol from our bloodstream to synthesize VitD - and that’s another side benefit ;-).

But that's something to keep in mind too: with the big scare around cholesterol levels, there are many people walking around on cholesterol medication who have artificially depressed levels of cholesterol. This doesn't just impact VitD production, but a wide array of cholesterol-derived hormones, such as testosterone.

Without getting too geeky about translating what this production means in terms of our daily needs, suffice it to say that this kind of sun exposure is sufficient to provide 90% of the daily needs for us humans.

HOWEVER:

  • This assumes that we get 30min of exposure DAILY
  • This assumes the quality of sunshine we get is good: i.e. that UV rays are not blocked by smog, pollution etc
  • Sunscreen (even SPF8) will block UV rays and reduce VitD production by up to 95%!
  • However burned skin from too much sun exposure has a similar effect: the skin would be so damaged that VitD production is almost completely impaired
  • Glass partially blocks UV rays, so sitting behind a window does NOT count
  • This assumes that our skin is “fair”: for really tanned people and individuals with darker skin, longer exposure would be needed as the darker the skin, the less UV rays reach the levels of the skin needed to activate synthesis of VitD




Note on sunscreen: there are some supplements (taken orally) that enhance your skin’s ability to protect you from the sun, which would still allow you to synthesize VitD from UV exposure without increasing the risk of melanoma (skin cancer). Contact me if you’re interested in finding out more.






hmmmm, but we live in Dubai, where’s it’s practically sunny year-round, so do we need to worry about this?

Well in my personal opinion, we absolutely must worry about this, and here is my reasoning as to why:


  • We spend the vast majority of our time indoors or behind glass windows
  • We (endurance athletes) tend to train either very early in the morning or late at night, and therefore we do not get optimal UV exposure
  • Let’s face it: many days in Dubai suffer from smog/humidity/pollution, all of which significantly filter our the UV rays we need


Yeah ok fine, so what do we do about it?

Sucking on those UV Rays:

Well, tricky question: I could tell you to go sit in the sun for 30min every day, but that’s hardly a practical solution for any of us right? And even then, that’s what’s recommended for the average person – you would need more as an athlete. But then sitting in the sun for 60min without sunscreen brings on other risks: sunburn, melanoma (skin cancer), etc.

(in fact, technically, the optimal exposure timeframe is between 10:00am and 3:00pm as that is when UV rays have the optimal wavelengths, again hardly a practical solution for most).

Yeah so no, that doesn’t work.

For those who can afford the time and expense, you can however use a sunbed for 10min. There is evidence out there from a number of studies showing that exposure to UV rays from sunbeds are just as good at triggering VitD synthesis in the body as UV rays from sunlight. Also, such rays are more concentrated, so you need less exposure vs. sitting in the sun.



Ok what about Vitamin-D-rich foods?

Well again sorry to burst your bubble but there are no “Vitamin D-rich foods” per se. There are some which have more than others, and there are some “VitD fortified” products (if you’re into such products). But neither really help significantly in remedying a deficiency.

As a guideline:
  • Vitamin D2: very hard to find in foods. There is some evidence pointing to Vitamin D2 synthesis in certain types of mushrooms when exposed to UV light, but I doubt that any of us are going to pick up a box of button mushrooms from Spinney’s and leave it outdoors (let me know if you attempt that J)
  • Vitamin D3: fish liver oils, fatty fish (salmon, sardines, etc), eggs, beef liver – industrially manufactured Vitamin D3 is sometimes added to certain fortified products such as bread, milk, juices, etc.

Oh, and one more important thing about this topic:
  • VitD is a “fat soluble vitamin”, so people with certain disorders such as Chrones Disease, Cystic Fibrosis, and Coeliac are at an even higher risk of VitD deficiency due to their impaired ability to metabolize fat.


Great, more pills to pop!!

Afraid so…

Outside of sitting in the sun, the only way to get sufficient VitD is through supplementation, and the best of the products out there is Vitamin D3: it is more readily absorbable and, in its existing form, it is more readily available to be “activated” in the body and start performing a number of functions related to bone health, immune system health, metabolic activity, etc.

So how much to take? Well there is no clear consensus once again, but here are some general guidelines:
  • Vitamin D Council: 5,000 IU/day
  • Endocrine Society: 2,000 IU/day
  • Ben Greenfield (fitness guru): 5,000 IU/day
  • FDA: 600 IU/day (but then again, typically all of their recommendations are quite low)
I personally take 4,000 IU per day split over 2 doses.

A couple of comments about these guidelines:
  • These are recommendations for the general population, so I don’t see a risk with athletes abiding by them
  • These recommendations are for “maintenance” of adequate VitD levels, and chances are we are all deficient – so it will take a while before we “replenish”
  • Given the increased demands on our bodies from endurance training, I would suggest to combine supplementation with frequent exposure to UV (either sun or sunbeds)
  • There are some liquid (spray) forms of Vitamin D3, which is more rapidly absorbed sublingually (under the tongue) when compared to pills/capsules which need to be digested


Too much of a good thing?

Healthcare professionals rarely advise people against “taking too many vitamins”. The reason for that is that most vitamins are water-soluble. In other words, your body will use what it needs and will get rid of the excess through urine.

HOWEVER, VitD is a “fat-soluble” vitamin. This means that you cannot excrete it through urine, and your body will have a hard time disposing of excess levels. (It’s an even bigger risk with fat-soluble Vitamin A).

Having said that, it’s “really hard” to reach such a level of VitD concentration where it becomes dangerous (technically it’s not the VitD concentration that’s dangerous but the associated increase in calcium concentration in the blood).
  • Your body’s primary way of regulating VitD will be by reducing the synthesis of VitD in the skin – and since 90% of your VitD is produced by the skin, that plays a big factor in regulating concentration
  • Studies have shown that it takes 20,000 IU to induce toxicity in rats, 3 million IU to be fatal in dogs! You do the math! Untested data point towards 600,000 IU to reach toxic levels in humans (trust me, that’s a lot of pills!)
  • Both the Vitamin D Council and the Endocrine Society set upper limits at 10,000 IU per day (for an average 400 IU VitD pill, that’s 25 pills!)


ADDITIONAL READINGS

UK study January 2009 on 1414 caucasian females

  • Significant correlation between levels of VitD and (i) sunbed exposure and (ii) long holidays in sunny climates. Higher correlation for holidays vs. sunbed exposure
  • Negative relationship between sunburn and levels of VitD. Sunburned people tend to have lower VitD (body unable to synthesize VitD from UV rays)
  • Positive correlation between tanned skin and VitD levels in Caucasians
  • Studies have shown that overall Vitamin D levels are lower among ethnic groups with darker skin (e.g. African and Sub-Continent) but this does not neccesarily affect bone-health: studies have shown that African-American women have higher bone density due to other genetic factors
  • Studies have shown higher incidence of osteoporosis among women in North Europe and UK vs. Southern Europe

August 2012 published 10-year observation of 9146 individuals in Denmark

  • Significant correlation between VitD levels and death caused by certain diseases:
    • Respiratory diseases
    • Digestive diseases (e.g. liver and kidney disease)
    • Endocrine diseases
    • Nutritional and metabolic diseases (e.g. obesity, diabetes)
    • Cancer
    • Cardiovascular diseases
    • Mental disorders (e.g. dementia, depression)
  • VitD essential regulator of Calcium homeostatis and bone minerlization – it is hormonally active
  • It is metabolized in the liver and kidneys to its active form, a steroid hormone