High Cholesterol? ….. Then feast on this!
by
Kathryn Alexander

To most of us high cholesterol equals heart disease – the number one killer in the Western world – or should I say amongst the affluent societies that have adopted a refined, high sugar, high fat diet. Invariably medical advice is to reduce the intake of dietary cholesterol and fat – and while this may be sound advice for the minority (those genetically predisposed to defective cholesterol clearance, usually diagnosed quite early on), for the majority this advice does not address the real issue which centers on insulin metabolism (rather than cholesterol metabolism) and would be more appropriately labeled “age-onset high cholesterol.”

The Feast and Famine Metabolism

Insulin is part of our “feast and famine” metabolism: in times of feast we can store the excess as fat and in times of famine we can draw on these reserves. In a feast and famine society (such as the indigenous Aboriginal and Polynesian cultures) greater survival advantage is conferred on those who are the most energy efficient – that is those who can store the greatest amount in times of feast to tide them over in times of famine. When these cultures adopt a “feast life-style” their systems automatically go into overdrive and we see the rapid onset of obesity, diabetes and heart disease.

The Western world has obviously adapted to the feast-only life-style – but, as statistics indicate, to a limited degree. For example, the first recorded death from heart disease was in 1910, now it is the leading cause of death; and in the last fifty years diabetes has risen from  0.002% (1 in 50,000) to 5% (1 in 20).  

The Insulin-Cholesterol Connection

Let’s take a closer look at the insulin-cholesterol connection. When we consume a diet high in refined carbohydrates (sugar and bakery products), its energy is released quickly and glucose floods the circulation instigating the release of insulin to counter this rise in blood sugar. Insulin is a storage hormone that “unlocks” the cells enabling glucose to enter. This brings the blood sugar levels down to within the normal range. Once inside the cell, glucose will either be used as fuel or stored as fat, which provides a good resource for energy when supplies are low. 

However, when the feast metabolism is continually thrashed by high-energy foods, the cells stop responding to insulin – in other words they won’t let insulin open the door to allow glucose in. This is known as insulin resistance and the upshot is elevated blood glucose and insulin levels. This starts a whole cascade of events as raised insulin levels trigger both cholesterol and triglyceride synthesis, and we see a new picture emerging.

The liver tries to keep abreast by removing the glucose (which it promptly converts to fats – triglycerides and very low density lipoproteins [VLDLs] - to be shipped out into the circulation) and degrading the excess cholesterol to bile acids for its elimination. But if the insulin metabolism remains switched on, then cholesterol and triglyceride synthesis continues unabated.

Oxidation - the final nail!

We then see superfluous glucose, triglycerides, cholesterol and lipoproteins in the circulation. Excess glucose will react with proteins in the blood vessel walls (glycation). This initiates a cycle of inflammation and oxidation which damages the blood vessel walls and adjacent nerves. The cross linking of protein-glucose complexes results in the formation of advanced glycosylated end-products (AGEs!) which represents nothing less than a build-up of inflammatory scar tissue that narrows the small capillaries reducing both blood flow and nerve transmission.[1, 2]

A similar process occurs with cholesterol. Cholesterol is a powerful anti-oxidant and in the absence of adequate anti-oxidant reserves (vitamins A, C, E and beta-carotene) will pick up free radicals and become oxidized. Once oxidized, specific immune cells take up the damaged cholesterol but in the process become engorged and turn into “foam” cells. These are sequestered in the blood vessel walls and - you guessed it – inflammation and oxidation is initiated, scar tissue forms which leads to the hardening and narrowing of the arteries. So the end result of insulin resistance is elevated cholesterol and glucose, the narrowing of the major arteries and small capillaries, a reduction in blood supply to the tissues, raised blood pressure, all increasing the risk of heart disease and diabetes. 

 What can we do?

 My first advice it not to let it get to this stage as it is difficult to reverse. For our younger readers make sure you follow the steps below, and in particular give your children the benefit of healthy eating habits which will stand them in good stead for life.

 We need to stop triggering the feast metabolism. This is easy:
         Try not to overeat
         Take 3 meals a day with a decent fasting period between each meal – this means no snacking
         Choose complex carbohydrates (unrefined cereal grains, legumes) as your source of energy. These foods release their energy slowly and do not stimulate a rapid surge in insulin

 Protect against oxidative damage. Include freshly prepared organic vegetable juices in your daily routine. These will supply you with sufficient anti-oxidants to protect your cholesterol, and generally reduce oxidative stress and inflammation in the system. (See Oxidative Stress – the Silent Inflammation for further tips on reducing oxidative stress).

 Exercise frequently. Under these circumstances glucose can be taken up without any requirement for insulin. (How about investing in a skipping rope?)

 Nutritional supplements may support cholesterol and glucose metabolism but generally they may be largely ineffective particularly if dietary modifications remain inadequate. Fats, refined carbohydrates and stimulants (tea, coffee, alcohol) are greedy for nutrients and will draw on your reserves for their metabolism. So while we may support a deficient diet with supplementation, and subsequently reduce our health risks, there is little suggestion that supplements can actually reverse the disease process. Pharmacological doses of niacin (active vitamin B3 – not its inactive counterpart nicotinamide) may be of benefit in reducing your LDLs (low density lipoproteins) and chromium may support the insulin/glucose pathway.

 Stay off the alcohol as this exacerbates insulin resistance.

 If you already have high cholesterol levels, you may need to remove foods that are high on the Glycaemic Index. This index measures foods by how quickly they release their glucose upon digestion.  The quicker the release, the greater the insulin response. Pure glucose is given the highest score of 100. Cooked parsnips (97), potatoes (83), and swede (72) fare badly, as do dried fruits (dates, 98) and watermelon (72). Of the grains, cooked barley comes out the best (25) with millet at 70. Don’t be too tempted to cut down your juicing regime, but perhaps opt for green juices rather than the carrot and apple juice. You can always substitute some celery for the apple when making your green juices.

 Medical drugs. Be aware that the contraceptive pill, HRT, and the corticosteroids all exacerbate insulin resistance. They oppose the action of insulin and inhibit glucose uptake by the cells. Remember that natural cortisone is also released in stress and will have a similar effect on glucose metabolism. Certain blood pressure medications such as the thiazide diuretics and the beta-blockers can cause or exacerbate hyperlipidaemia. [3]

If it all seems too complicated just cast your mind back (or use your imagination) to pre-processed, pre-long shelf-life foods. What did we eat? Fresh, organic, unrefined foods with a strong life-force and active nutrients. One of my favourite sayings is “Eat foods that spoil, but eat them before they do.”  If you invest now, you will save later – as one patient of mine recently said, “If you think the cost of health is expensive – try disease!”

1. www.researchd.com/neuroabs/rageb.htm
2. Cerami, A., Vlassara, H., Brownlee, M., “Glucose and Aging,” Scientific American, 265(5), 1987, pp 90-96
3. William J Marshall: Clinical Chemistry, 2nd edition, Gower Medical Pulishing, ch 16 “Disorders of Lipid Metabolism.”