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What’s problems?

Sex Hormone Binding Globulin (SHBG) The average person gets their bloods, looks at total testosterone and thinks they have all they need to know. SHBG decides how total testosterone should be read. So what is it? SHBG is the protein made in your liver that binds testosterone and oestradiol (E2) and carries them round the body in your blood. Testosterone bound to SHBG is held in reserve. It isn’t acting on anything. Just under half of your testosterone is held tightly by SHBG. Just over half is held loosely by albumin. This is the most common protein in the bloodstream, and testosterone bound to albuman can unbind and be used. Only about 2% is completely free. A high SHBG can give you a normal total T and very low free T. Low SHBG can give you the opposite. The free testosterone on your report is usually calculated from the total, SHBG and albumin using an equation. Any change in SHBG moves free T, even if your production hasn’t changed at all. The free androgen index (FAI) is simpler still. It’s just total testosterone divided by SHBG, with no albumin. FAI overestimates more and more the lower SHBG goes (it’s usually used in women). Low SHBG goes hand in hand with obesity/insulin resistance, and TRT pushes it down too. So what moves SHBG? The liver has a control switch that sets how much SHBG it makes. What sets that switch is how much new fat your liver is making, and high insulin drives that. More fat being made means less SHBG. That’s why fatty liver, obesity and insulin resistance all push it down. Androgens binding to androgen receptors on liver cells telling them to stop making SHBG. T3 can push it up but most people taking T3 won’t see a noticeable change (more on this in a future post).  Oestrogen and older age can also push it up (the age thing is more nuanced though). Liver disease can go either way. Cirrhosis raises it, but fatty liver, which is far more common, lowers it. Obesity and insulin resistance cause low SHBG. What we don’t know is whether SHBG itself does anything, or if it’s just the warning signal for the liver. The warning light has a good argument. TRT pushes SHBG down but in trials liver fat went down or stayed put rather than going up. If a low SHBG drove fatty liver that wouldn’t happen. And nobody has ever run a trial raising SHBG on purpose to see if anything improves (likely because it would be very difficult to raise SHBG without other variables since you can’t just give some more SHBG). A higher SHBG within reason isn’t a bad thing either. Thyroid hormone pushes it up, and that’s your body moving hormones to where they need to go. And we know that T3 signals abundance to the rest of the body (within reason).  Lose a lot of weight and SHBG goes up as liver fat reduces and insulin resistance improves. Total T increases too but with SHBG also increasing overall you might not see a change at all. Another underrated but important factor is that biotin supplementation can give a false low SHBG reading which will affect your Free T. Everything else on SHBG, free testosterone and FAI is in our Biomarker Guide on n1health.co.uk/pages/biomark…

Not thoroughly convinced persimmon is a real word

Persimmon will always be one of the most underrated fruits and I’m okay with that because that means more for me

Our phlebotomy partner has almost 300 clinics all over the UK. And more are being added every single day. We’ve added a clinic finder to the site so you can see exactly how far the nearest clinic will be from you before you buy. n1health.co.uk/pages/find-a-…

HbA1c Most people think HbA1c is their average blood sugar over the last 3 months. It mostly is. Haemoglobin is the protein inside your red blood cells that carries oxygen. Sugar in your blood sticks to it (glycation), and HbA1c is how much of it has stuck. So Hb = Haemoglobin. A = Adult. 1c = glucose locked onto the end. (you can also have 1a or 1b which tell you fructose based sugars or pyruvate are locked on instead). Red cells live about 120 days and keep picking up sugar the whole time. Initially the glucose only binds temporarily. But if it stays there long enough, it becomes permanent and stays for the whole life cycle of that red blood cell. At any one point you’re carrying red cells of every age, from brand new to about 4 months old. Most of them have been around for the last few weeks, but only the older ones were around 3 months ago. So the result essentially covers the last 2-3 months. Also, just because 120 days is how long a red cell can last, it doesn't mean that's how old yours are on average. The average age runs from ~38-60 days. Older cells have had longer to glycate, so if yours last longer your HbA1c can read higher at the same blood sugar. This is the reason 2 people with diabetes can have the same HbA1c but average blood sugars over 3 mmol/L apart. (That’s the difference between a fasting glucose of 5.0 and 8.) So anything that changes how long your red cells last changes the number. In iron deficiency anaemia the red cells end up older on average which means more glycation. So without moving blood sugar, your HbA1c can go up. The worse the anaemia the bigger the effect. (UK results are in mmol/mol and US ones are a % btw. 42 mmol/mol is about 6%.) A HbA1c of 42 with a low ferritin isn’t the same result as 42 with normal iron. Sort the iron out and repeat it. Donating blood or anything that breaks red cells down early does the opposite. Cells end up younger on average so it reads lower. A transfusion also drags it towards the donor’s blood sugar instead of your own. Where the line sits depends on which country you’re in. In the UK 42 to 47 mmol/mol (6.0 to 6.4%) is pre-diabetes. The American Diabetes Association starts prediabetes at 39 (5.7%). 48 (6.5%) is diabetes in both. But if you’ve got no symptoms they usually want a second test to confirm it. Below 42 nobody anywhere sets an 'optimal' number. Results usually need to be roughly 4 to 5 mmol/mol apart before the change is probably real. As with most tests, its best to stick to one lab. Each lab is allowed to be up to 5% either side of the true value on the US % scale, which is about 3.6 mmol/mol either side of 48. So 2 labs that both pass their quality checks can report the same sample as 44 and 52. Lower isn’t automatically better either. In large population studies the lowest death rate sat at about 36 to 38 mmol/mol. Risk went up above about 46 and also below about 31. A very low HbA1c tends to come with anaemia, higher liver enzymes and lower body weight. So it’s probably a sign of something else going on rather than the cause. Everything else on HbA1c, including how ethnicity and inherited haemoglobin differences like sickle cell trait change it, is in our Biomarker Guide on n1health.co.uk/pages/biomark…