Weight loss; when it's hard

This post is a set of jottings on weight control when it's difficult. It's essentially unreferenced and was produced in response to the enquiry by Windmill/Windmum (same person) in the comments after this previous post.

Many posts ago I mentioned the thought that it was probably perfectly possible to gain weight on a low carb/high fat diet, provided there were adequate calories involved. Because insulin appears to be very important in controlling the activity of lipoprotein lipase, that enzyme which gets fatty acids out of lipoproteins and in to fat, there has to be some other way of doing this transfer when insulin levels are low.

Chris found the enzyme, it's ASP. You can read more here. ASP is Acylation Stimulating Protein. Let's stick to ASP.

This is completely logical. Those of us who eat combined high fat with LC tend to have rather low levels of insulin in our blood stream. Low levels of insulin mean low levels of activity in the lipoprotein lipase just outside our fat cells. If there was no other way of getting fat out of chylomicrons or VLDL particles and in to adipocytes, we LC eaters would be as chronically hypertriglyceridaemic as a diabetic on a low fat diet. No one would want that.

In to the gap steps ASP, which allows us to store the fat from our current meal as adipose tissue for use in the time before our next meal. On intermittent fasting or once daily eating we HAVE to store an awful lot of fat until we next eat. ASP gets fat in to adipocytes for us, without needing an insulin spike. Good.

What gets the fat out of adipocytes? That's hormone sensitive lipase (HSL from here onwards). Actually, even in HSL knockout mice it is quite possible to get fat out of adipocytes and in the circulation. Which system does this I've no idea and, because none of us is a HSL knockout mouse, I don't much care! If HSL is really working well, it will do the job.

So, say we are eating once daily, we can assume ASP will store any fat we eat in excess of our immediate needs, tucked in to our adipocytes. What reduces our weight is when the release of free fatty acids (FFAs) from our adipocytes via HSL is greater than the input via ASP.

Getting FFAs out easily means optimising the activity of HSL. That means lowering insulin. Low insulin allows HSL to work effectively. An effective HSL supplies FFAs to allow our metabolic activity requirements to be met from adipocytes. A freely available energy supply from adipocytes should reduce the need to obtain energy from food, ie less hunger. Ineffective HSL means you need to eat more, because your fat cells are hanging on to their contents. To paraphrase the whole of Good Calories Bad Calories in one phrase:

Excess weight is the result of a failure of adipocytes to release energy, hunger is needed to supply any shortfall needed for metabolism.

Working on this basis, the requirement for weight loss must be to minimise insulin. This allows metabolism to run on the surplus of adipose tissue energy released over dietary energy consumed. On a high fat diet with low insulin levels ASP will still rapidly store most meal derived fat, HSL will subsequently release it as needed.

Ultimately weight loss boils down to lowering insulin levels. So we end up with a need for minimal carbohydrate. On the Optimal Diet basis that would be the lowest amount for a sedentary person to avoid ketosis, say 0.5g/kg of "ideal" weight. If a person is well adapted to a LC/high fat diet then protein requirements can be as low as 0.8g/kg ideal weight. Protein metabolism requires some insulin response and any excess protein will be mostly converted to glucose, which requires a considerable amount of insulin to be used. Fat intake should be relatively low (by Kwasniewski standards only!) to keep total calories below those needed by our metabolism, otherwise ASP will store more fat than HSL will release. HSL will only ever release enough FFA for the metabolic needs in a healthy person.

On top of that basic plan, the basal metabolic rate must be normal. If a person is hypothyroid they will require far less FFAs for their metabolism and so HSL will adjust to this and minimise fat break down. ASP won't, so a high fat diet will produce weight gain if calories are in excess of metabolic needs. Correct and well monitored thyroid medication is needed for this. As most common thyroid problems seem to be auto immune in origin, avoiding gluten seems like a good idea, if it isn't always a good idea. Which it is. BTW both hypo and hyper thyroidism appear to cause insulin resistance. That seems a bit bizarre to me, but there you go.

There seem to be a few teaks available. Tinkering with insulin sensitivity may be worthwhile. If your muscles need a certain amount of insulin to dispose of a given amount of glucose, then the pancreas will produce that insulin. In addition to helping the muscles take up glucose that insulin will inhibit FFA release from adipocytes. Resistance exercise seems to be the best way to increase insulin sensitivity. Doing this shifts that same given amount of glucose on less insulin. Less insulin means less inhibition of HSL, so easier fat loss.

Improving insulin sensitivity can also be achieved by avoiding medication which interferes with the action of insulin. There has to be a balance here. If dumping your antidepressant makes you suicidal, don't do it! Most blood pressure medications can be gradually reduced as blood pressure tends to normalise on LC eating. Corticosteroids are a real bugbear. Again, if they are life saving you have no choice, keep taking them and accept the weight they make you carry. If you are corticosteroid dependent, never forget that acute withdrawl can be fatal.

If you live as far north as Finland then checking and correcting your vitamin D status would be well worth while.

Anyone reading Chris or Emma's blogs will realise that aspirin, and possibly other related salycilates from plants, cause the pancreas the secrete extra insulin. Avoid. Gluten and wheat germ agglutinin (both from wheat, barley and rye) are (or contain) insulin mimetics, avoid. Casein stimulates insulin secretion, avoid. Pharmaceutical NSAID probably do the same as salycilates, avoid if possible.

Coconut oil is interesting. It has a reputation for assisting weight loss, but if gavaged in to the stomach of a chow fed lab rat it will decrease blood glucose and increase blood insulin levels. You don't want to increase your insulin levels if you want to loose weight. There are other plus and minus sides to coconut oil, but I'd keep life simple and avoid it.

That's quite a list. There are probably loads of other tweaks that I've not thought of...

If you are in the same position as Windmill, that must all be pretty depressing to read. If you want to adjust your weight downwards to where you would like it to be, you are stuck with a pretty extreme version of the Optimal Diet, low but adequate in protein, low in carbs, probably eaten as starches as part of the evening meal, fine tuning your thyroid meds and replacing coconut oil with lard. Lard at a moderate level that is. Do everything practical to maintain your insulin sensitivity.

This seems to work (from an off blog comment from Windmill).

The trouble is that it is HARD. This is not OD as myself or Stan eat it. This is kitchen scales, bathroom scales, portions, calculations, limitations, problems eating out, vegetable avoidance, cheese avoidance, gluten avoidance....... Arghhhhhhh

So there is a trade off. It's one hell of a big trade off. Some of us (most of us probably) have it easy, certainly easier than Windmill. But ultimately there is that balance between fats in to adipocytes and fats out of adipocytes. ASP and HSL. Even worse, there is a trade off between what you know you can do, that you have already done successfully in the past, and the real bind of allowing your diet to rule your life and putting some pretty draconian limits on your eating. Does anybody want to do this? Long term, for ever? That's a very personal decision.

Also the final thought must be: What is the healthiest weight, personal preferences aside?

I don't think we know.

Peter