Science Who'll dare to face the facts on obesity and Covid-19? - With each day that passes, we learn a little bit more about the nature of this ghastly virus. Statistics show that obesity is one of the biggest risk factors for Covid-19

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With each day that passes, with each new grim death toll, we learn a little bit more about the nature of this ghastly virus.

This week in particular, statistics have come to light showing that obesity is emerging as one of the biggest risk factors for Covid-19.

According to data released by the NHS, being overweight raises the chances of dying in hospital from the illness by 40 per cent.

Having a body mass index of between 30 and 34 makes a person almost twice as likely to be admitted to ICU as someone with a BMI under 30. For those with a BMI of 35 or more, the likelihood is nearly four times higher.


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Obesity is emerging as one of the biggest risk factors for the coronavirus pandemic

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Data shows have a 40 per cent more chance of dying in hospital from coronavirus if you are overweight, according to NHS data

This is a very tricky piece of information for the Government to handle. Obesity is a highly politicised issue: ‘fat-shaming’ is one of the more heinous crimes against political correctness.

The notion that the medical establishment is acutely aware of the newly discovered risks of obesity, yet fearful of talking about it, was reinforced by a conversation I had last week with a friend who is a leading bariatric surgeon.

‘It’s a very difficult subject to broach,’ he told me, ‘and no one quite wants to say it, but there’s no question in the mind of any of my colleagues: patient size is a major factor in this disease.’

As the UK has the highest proportion of seriously overweight people in Europe, this is of grave concern. Yesterday, an NHS report said 67 per cent of men and 60 per cent of women here are overweight or obese.

It means that as a population in general, we are inherently more at risk of dying from coronavirus.

Yet persuading people to accept that their weight can be a major health issue is very hard indeed.

That is because size is deeply bound up in psychological issues and self-esteem. Fat people, as I know from a lifetime’s struggle with the scales myself, can be very defensive about their condition. We interpret any concern about our weight as negative criticism, an attack on our identities.

Big people — and in particular bigger women — have become so sacred that none but the most bigoted would dare criticise.

I know how joyless life can be when you feel — as so many do — that your only friend is the tub of ice cream in the freezer. That is why I’ve always felt that obesity was in effect an eating disorder that needs to be managed as much in the mind as in the body.

For any politician — especially a lean male such as Health Secretary Matt Hancock — to have to step into this minefield is tough. It’s hard enough having to ask the over-70s to shield themselves; can you imagine the hysteria if he asked the obese to do the same? Or suggested that people should isolate according to their weight, rather than their age?


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Can you imagine if Matt Hancock asked people struggling with obesity to shield themselves and social distance from the virus like he has done with the over-70s?


But if the science is correct, maybe that should be the strategy.

Because there is one fundamental difference between the obese and the over-70s. Age is not a choice. Size, ultimately, is.

For the past six weeks, the nation has talked of nothing else but ‘saving our NHS’. Yet for a decade we have been bringing the NHS to its knees by refusing to take personal responsibility for obesity.

It puts us at increased risk of developing cancers, high blood pressure and type-2 diabetes — conditions that cost the health service billions of pounds a year.

So if we really want to protect the NHS, those of us who are overweight or obese can start by taking a deep breath, stepping on those scales and beginning the long, hard journey back to health.

The virus may be tailing off now but a second wave is expected in the winter. There are a good few months between now and then.

If you can be inspired to lose weight, you might not only help to save the NHS. You might just be saving yourself.

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So it turns out that Corona-chan is the answer to the Fat Question. Fatties BTFO.
 
Comfort eating is a reaction to low serotonin (a neurotransmitter whose deficit causes depression, although other neurotransmitter issues can also cause depression). Eating carbs triggers an insulin surge, which causes the muscles to increase their uptake of branched-chain amino acids (BCAAs). BCAAs are one of two groups of amino acids transported across the blood-brain barrier (BBB) by the large neutral amino acid transporter (LNAA). The LNAA transports BCAAs and aromatic amino acids (AAAs) at a rate determined by their relative presence in the bloodstream. Thus, as BCAAs become less available due to muscular uptake, the transport rate of AAAs increases.

The AAAs are phenylalanine, tyrosine, and trytophan; the latter is converted to 5-hydroxytryptophan (5-HTP) inside the neurons, which then in turn is converted to serotonin and helps you feel good, or at least not terrible. Thus, raising insulin indirectly results in increased synthesis of serotonin.

The other two AAAs can be converted to dopamine, the neurotransmitter whose release is associated with pleasure and reward, so that's the other part of the reason that eating carbs feels good. Dopamine is in turn converted into the neurotransmitters norepinephrine and epinephrine, associated with alertness, attention, and activity, so there is at least a theoretical basis for sugar to lead to hyperactive symptoms in some children; there are genetic variations in the rate of conversion of dopamine to norepinephrine. (Sugar has also been shown to lead to a short-term increase in cognitive performance, which might be caused in part by this mechanism.)

Anyway, as it turns out, you can boost 5-HTP (and thus serotonin) in other ways if you don't want to get fat and diabetic. 5-HTP is an over-the-counter nutritional supplement in the US which has been shown to reduce carb consumption in some studies. Many people also have low serotonin because they have deficiencies in the nutrient cofactors for serotonin synthesis, which include zinc, magnesium, and vitamin B6. Basically, a lot of people are fat because poor nutrition means that eating carbs is the only way they can feel better. Gut dysbiosis can contribute to obesity too; for example, by secreting chemicals that make you feel like crap when you don't feed your gut yeast the simple sugars it craves. Overgrown gut microbe populations can also block nutrient absorption by damaging the gut lining and by stealing nutrients for itself. So are there treatable, medical reasons why some people want to eat too much. But the first step is always admitting that you have a problem.
 
Comfort eating is a reaction to low serotonin (a neurotransmitter whose deficit causes depression, although other neurotransmitter issues can also cause depression). Eating carbs triggers an insulin surge, which causes the muscles to increase their uptake of branched-chain amino acids (BCAAs). BCAAs are one of two groups of amino acids transported across the blood-brain barrier (BBB) by the large neutral amino acid transporter (LNAA). The LNAA transports BCAAs and aromatic amino acids (AAAs) at a rate determined by their relative presence in the bloodstream. Thus, as BCAAs become less available due to muscular uptake, the transport rate of AAAs increases.

The AAAs are phenylalanine, tyrosine, and trytophan; the latter is converted to 5-hydroxytryptophan (5-HTP) inside the neurons, which then in turn is converted to serotonin and helps you feel good, or at least not terrible. Thus, raising insulin indirectly results in increased synthesis of serotonin.

The other two AAAs can be converted to dopamine, the neurotransmitter whose release is associated with pleasure and reward, so that's the other part of the reason that eating carbs feels good. Dopamine is in turn converted into the neurotransmitters norepinephrine and epinephrine, associated with alertness, attention, and activity, so there is at least a theoretical basis for sugar to lead to hyperactive symptoms in some children; there are genetic variations in the rate of conversion of dopamine to norepinephrine. (Sugar has also been shown to lead to a short-term increase in cognitive performance, which might be caused in part by this mechanism.)

Anyway, as it turns out, you can boost 5-HTP (and thus serotonin) in other ways if you don't want to get fat and diabetic. 5-HTP is an over-the-counter nutritional supplement in the US which has been shown to reduce carb consumption in some studies. Many people also have low serotonin because they have deficiencies in the nutrient cofactors for serotonin synthesis, which include zinc, magnesium, and vitamin B6. Basically, a lot of people are fat because poor nutrition means that eating carbs is the only way they can feel better. Gut dysbiosis can contribute to obesity too; for example, by secreting chemicals that make you feel like crap when you don't feed your gut yeast the simple sugars it craves. Overgrown gut microbe populations can also block nutrient absorption by damaging the gut lining and by stealing nutrients for itself. So are there treatable, medical reasons why some people want to eat too much. But the first step is always admitting that you have a problem.
Is that why SSRI’s cause sugar cravings?
 
Is that why SSRI’s cause sugar cravings?
I believe the issue with SSRIs is that they alter zinc regulation; many of the potential side-effects, such as loss of libido and suicidal depression, match the symptoms of low zinc. Animal studies show that at least some SSRIs shift zinc from the tissues (such as the brain) to the bloodstream. Animals fed a low-zinc diet experienced drops in plasma zinc levels, which were reversed by SSRIs. But where did the zinc come from, since they were on a low-zinc diet? Obviously, it had to have been pulled out of the tissues into circulation. I also believe this because I've taken a number of different SSRIs, and all caused low zinc. (I've experienced extremely low zinc before, so I know exactly what it feels like. I know it was low zinc because the symptoms resolved very quickly once I started taking zinc supplements.)
 
Literally everyone except the fats.
 
I believe the issue with SSRIs is that they alter zinc regulation; many of the potential side-effects, such as loss of libido and suicidal depression, match the symptoms of low zinc. Animal studies show that at least some SSRIs shift zinc from the tissues (such as the brain) to the bloodstream. Animals fed a low-zinc diet experienced drops in plasma zinc levels, which were reversed by SSRIs. But where did the zinc come from, since they were on a low-zinc diet? Obviously, it had to have been pulled out of the tissues into circulation. I also believe this because I've taken a number of different SSRIs, and all caused low zinc. (I've experienced extremely low zinc before, so I know exactly what it feels like. I know it was low zinc because the symptoms resolved very quickly once I started taking zinc supplements.)
Aren't SSRIs used to treat binge eating disorder, food addiction and almost any mental illness that doesn't have an FDA approved treatment? And Wellbutrin is used for getting the brain to make more dopamine. If binge eating behavior is caused by chemical imbalances in the brain, wouldn't these medicines treat it? Is zinc tested for on routine bloodwork? On the backs of zinc supplements they always warn of copper deficiency but I don't know how common that is.
 
Aren't SSRIs used to treat binge eating disorder, food addiction and almost any mental illness that doesn't have an FDA approved treatment? And Wellbutrin is used for getting the brain to make more dopamine. If binge eating behavior is caused by chemical imbalances in the brain, wouldn't these medicines treat it? Is zinc tested for on routine bloodwork? On the backs of zinc supplements they always warn of copper deficiency but I don't know how common that is.
SSRIs multiply the effect of serotonin at the same time they lower zinc, and how much of each effect they have varies both on the drug and the person. So it is possible that someone who gets the serotonin boost with little adverse impact on zinc could in fact end up eating less. Also when zinc gets very low you stop wanting to eat at all, but again the symptoms of low zinc vary somewhat by person. It's quite complicated and poorly understood.

Copper deficiency can be avoided by taking a small amount of copper (2 mg or so) daily. In fact some zinc supplements also contain copper for exactly this reason. Women have a higher copper uptake due to higher estradiol, which increases the body's ability to absorb copper from food.
 
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