Not tonight, honey. I’m exhausted.

Have you heard the term ‘ironman widow’? Where someone’s husband (or wife) is basically invisible for the better part of 12 weeks as they prepare for an upcoming race. This not only relates to being physically present (which is diminished when the training time is upwards of 15-20h a week) but also ‘present’ when at home. Often exhaustion sets in, particularly nearer the end of the week or after a heavy training day, where the mere thought of moving from the couch is akin to another 6h ride. Sex? Don’t even go there. It’s a fairly common (yet usually unspoken) phenomenon that rolling around in the sack is off the agenda in the lead up to the event. And I’m not talking about the day before an event; it’s more like as a general rule because they are too damn tired. Does this sound familiar? Yes, being tired is a natural (and expected) part of the training cycle – however, much as we talk about adrenal fatigue and hormonal imbalance in women – this is not an uncommon occurrence in men. It’s just not often talked about.

When we talk hormones, I know that I’m guilty of just addressing women. You know – the stress hormones, thyroid hormones and sex hormones. However men are not exempt from the debilitating effects of overdoing it. Just as a ‘rushed’ lifestyle can affect the thyroid and sex hormones in women (including testosterone), men who undertake endurance sport are at risk of poor testosterone status.

Testosterone: a sex hormone (also present in women too) is a chemical messenger. It declines as we age, and some studies have found a that testosterone levels for a male in their late 30s are down by as much as 50 % on the levels that were present in their 20s. Just as oestrogen is controlled by the hypothalamus, it is the same for testosterone; when the hypothalamus detects a deficiency of testosterone in the blood, it secretes a hormone called gonadotrophin-releasing hormone (GRH). This is detected by the pituitary gland that in response starts producing follicle stimulating hormone (FSH) and luteinizing hormone (LH). These travel to the testes where testosterone is produced from cholesterol by the leydig cells with just a small amount produced by the adrenal glands. It’s then sent back into the blood stream and either attaches to sex hormone binding protein (SHBG) and becomes biologically inert, or remains free in the bloodstream.  Normal levels are between 300 ng/dl – 1200 ng/dl (10.41)-41.64 ng/dL. The three types of testosterone you might see reported are:

  • Total testosterone- As the name implies, it’s how much testosterone available and is the sum of free and bound testosterone.
  • Free testosterone is the most biologically active form of testosterone. Free but low biologically active test and therefore still have signs/symptoms of overall low testosterone.
  • Bound testosterone-This is the testosterone bound to the protein Sex Hormone Binding Protein (or Globulin) (SHBP/SHBG). A high amount of SHBG will usually indicate a low free testosterone.

Testosterone is not just important for reproduction and sex drive – it has a number of other roles including supporting bone mass, regulating fat distribution, muscle size and strength and red blood cell production. If you are a typical endurance athlete who tends to push themselves and have had stress fractures that can’t be put down to a lack of calcium, it could well be that low testosterone is a contributing factor. As we know, testosterone increases during training and contributes to overall energy levels; a low production of testosterone contributes to the fatigue that can be felt under a heavy training load, making someone feel worse than they should. It’s difficult though, to know what is a normal byproduct of a heavy training load (because, let’s face it, endurance sport requires longer and harder training than, say, golf). Below are some common signs and symptoms of low testosterone.

  • Decreased/absent early morning erection
  • Reduced sex drive
  • Erectile dysfunction
  • Loss of facial or pubic hair
  • Testicular atrophy
  • Low bone mineral density/fractures
  • Night sweats

Phew! That’s not you? Well, you may not be out of the woods just yet. Less specific (or earlier signs) include:

  • Decreased energy or motivation
  • Poor concentration and memory
  • Disrupted sleeping patterns
  • Moody
  • Reduce muscle/increased fat mass
  • Reduced performance

You can see that the early signs of a reduced testosterone level could be summed up by being a bit ‘tired’ and are fairly non-specific. The best way to know what is going on with your testosterone is to get it tested through your doctor (noting that the free testosterone is the important measure).

Thankfully there is plenty you can do with your diet to ensure you’re optimising your ability to produce testosterone without getting a prescription for the pharmaceutical type. Unsurprisingly, these come down to pretty much what I write about on a weekly basis:

  • Ensure adequate vitamin D – this is involved in the production of the corticosteroid hormones and it’s important we have enough available to support the production of our thyroid, stress and sex hormones. Food sources are full fat dairy products, a small amount in butter, liver, animal protein and fatty fish such as salmon, sardines and mackerel. Taking a supplement (that also contains vitamin K2) is warranted for a large part of the year in New Zealand, but particularly as we come out of winter and into spring, where the UVB rays are diminished and we’ve been spending the vast majority of time inside on the windtrainer to dodge the weather.
  • Ensure adequate zinc intake (through oysters and animal protein, and brazil nuts too) – a note here is that iron can reduce our overall ability to absorb zinc, and this may need to be looked at if you’re taking an iron supplement.
  • Ensure adequate selenium intake (seafood, Brazil nuts) and vitamin A (full fat dairy products, liver, eggs, animal protein)
  • Saturated and monounsaturated fat: Again, most of the foods mentioned above are good sources of saturated fat in the diet, and monounsaturated fat is found predominantly in olive oil, eggs, avocado and raw nuts. The reality is, all fats contain the range of fatty acids we need, and are labelled ‘saturated’ or ‘monounsaturated’ fats due largely to the amount they contain. Coconut oil (which has had some bad press of late, despite a lack of evidence of a relationship to heart disease) is particularly rich in saturated fat.
  • Cholesterol: another important co-factor in the creation of the sex hormones, and forms the backbone of these. Foods of animal origin help supply dietary cholesterol for this role. If you’re someone who has followed a low fat diet or vegetarian diet and has a low cholesterol level, then potentially your testosterone could be lower than ideal.
  • Ensure adequate B vitamins and magnesium also (present in the foods mentioned above and in abundance in vegetables).

Finally – on the life side of things: sleep more, ensure adequate recovery from training and have more sex. That will increase your testosterone.

Peter on cholesterol….pt 2

Following on from last week…. and trying to summarise Peter Attia’s cholesterol talk at AHS12 to illustrate why the cholesterol reading you get from Medlab doesn’t give you a good indication of your risk of atherosclerosis and subsequent heart disease. Cholesterol. The internal regulatory process responsible for cholesterol involves both the production of cholesterol and absorption of it. There are a few reasons why some people have higher cholesterol levels, and broadly speaking there are people who are good at producing cholesterol, and people who are good at absorbing it. The absorption of cholesterol is governed by a receptor in the gut which is responsible for allowing the movement of sterols in and out of the gut. There is also a receptor in the gut that is responsible for getting rid of all unwanted sterols (and excess cholesterol) from the gut to be excreted (called ABCG5 and ABCG8). It’s only ‘free’ sterols that are able to get in – esterified cholesterol (i.e. that which is delivered through food) is not able to enter the gut. For this reason there is very little, if any, relationship between cholesterol in food choices and our total blood cholesterol level. Health professionals have been aware of this for a few years now, however the general public is still confused and I can’t tell you how often I get asked the question of whether there is a limit on eggs. However some may have a defect with the receptor in the gut letting too many of the sterols in, or a problem with the ABCG5/G8 getting rid of the unwanted sterols. The effect this has on overall cholesterol homeostasis is not clear at this stage.

 I can't get enough of eggs, even the grumpy ones. (image from chelseacrockett.com)

I can’t get enough of eggs. (image from chelseacrockett.com)

While we hear a lot about LDL-cholesterol, the lipoproteins responsible for carrying HDL and LDL also carry triglycerides and phospholipids. These are produced by the liver and are known as Apo-A (HDL cholesterol) and Apo-B (LDL cholesterol). Apo-B lipoproteins contain more triglycerides than Apo-A lipoproteins, and include very low density lipoprotein (VLDL), which (when it sheds its triglycerides and phospholipids) converts to IDL (intermediate density lipoprotein) and LDL. VLDL contains more triglycerides than cholesterol (5:1 ratio) compared to LDL which is more in the vicinity of 4:1. When the VLDL are transported from the liver they release triglycerides and phospholipids and triglycerides to be used for energy by the muscles or stored in the adipose tissue. In people that are metabolically healthy, the triglycerides are delivered to the muscles by VLDL to be used for energy – however in those that have metabolic health problems, the triglycerides are more likely to be stored as fat. In addition, as they contain a lot of triglycerides, when we have high levels of processed carbohydrate we are going to have a lot more VLDL in our bloodstream as these excess carbohydrates are converted to triglycerides and packed up in the VLDL. Research has shown that the number of VLDL particles increases risk of athleroschlerosis. In addition, there is a lipoprotein Apo-E which is found in Apolipoprotein E (ApoE) is a class of apolipoprotein found in the chylomicrons (carriers of dietary fat after we eat) and Intermediate-density lipoprotein (IDLs) that is essential for the normal breakdown  of triglyceride-rich lipoprotein constituents such as VLDL, and there exists three main forms – E2, E3 and E4. These differ in the position of certain amino acids in the structure, but alters the function of the Apo-E lipoprotein significantly. Those people with the E2/E2 and E4/E4 expression have been found to be at greater risk of atherosclerosis.

The whole cholesterol issue is confusing. I spent about 3 hours writing that last paragraph and its very rough and actually probably didn’t mention 18 other ‘must knows’ in order to understand it properly. However, I think that, really, the most important thing to understand is that JUST knowing your LDL number (or total cholesterol number) is not going to provide you with a good idea of your risk of atheroschlerosis. Firstly – in NZ we aren’t able to quantify LDL – instead it is a calculated number based on the direct measurement of total cholesterol and HDL cholesterol. That’s an issue. However, moreso, there are certain conditions which can increase risk associated with cholesterol. The Apo-B lipoproteins can get into the sub endothelial space in the artery wall and can spark an immune response, causing inflammation. This inflammation can then increase the number of particles being delivered to the site (as LDL is released in response to inflammation) thus further particles get into the artery wall. The Apo-A lipoproteins, responsible for delivering HDL don’t.

Of course, inflammation is not just caused by one factor – and I bang on about this a lot in pretty much every health related post I write here and on my facebook page. The oxidation and glycation (binding of a glucose molecule to a protein) of the particles can change the functionality of the lipoproteins which causes them to damage the endothelial cells I mentioned above. These processes are caused by an overload of stress in the system: dietary, activity, toxins and the like. Result? Increased likelihood of atherosclerosis. Oxidised LDL can’t be measured in New Zealand but people can send their results to a laboratory in Australia to get this measured.

Another important factor is the size and the number of LDL particles in our system. There are two different patterns – and those with fluffy LDL particles (bigger) are less likely to get stuck in the artery all compared to the smaller (pattern B) particles, which are more atherogenic. It’s not just size that matters, though – it’s overall particle number. And when the size of the LDL particles have been controlled for, it suggests that overall the number of particles is more important. The greater the number of particles, the less able they are to move efficiently around the bloodstream, the more likelihood of being oxidised and subsequent inflammation.

Also important to consider that LDL cholesterol is used as a patch to help with inflammation in the body – if you have high LDL then that could very well be indicative of an underlying issue that needs to be addressed. Interestingly, while we’ve understood that a high HDL is a good thing and the higher the better, in fact a high HDL is not a get out of jail free card either. Indeed, trials that increase HDL levels through therapeutic means have been stopped before their planned end dates due to the lack of clinical benefit in people who have established cardiovascular disease. If HDL is high, then there may well be a reason outside of just eating a good quality diet. There are different forms of HDL and, its primary role is a carrier to remove excess cholesterol away from the blood vessel wall to be excreted, if it is not functioning correctly then that in itself can increase risk of heart disease (depending on other risk factors). If we use the car analogy (as people tend to do when it comes to cholesterol, quite useful), then if the car breaks down, then the cholesterol is not going anywhere – this is double-whammy bad actually, as it is unable to break down the plaque at the artery wall and in itself can cause inflammation.

Yeah. Cholesterol. So how useful are your own cholesterol readings? First – there are a couple of good ‘proxy’ measures that can be gleaned from your results to give you an idea of risk. Triglyceride/HDL can give you an indication of particle size. The smaller the ratio, the larger the particle size, the less risk. You need to calculate this as it’s not given to you. However, this may not be as important as total cholesterol/HDL, which can give you an indication of particle number. The smaller the ratio better and this is likely to be a better indicator of overall risk. Finally, and most importantly, is the context. As I said last week, our cholesterol readings are nowhere near as important as we once thought with regards to atherosclerosis and heart disease – and can’t be looked at in isolation of other risk factors. The context matters, so evaluate them in light of your current lifestyle to get a better understanding of their usefulness.