How Sugar Ages Your Brain

Excessive amounts of sugar damage the brain partly because it forms toxic compounds called ‘Advanced Glycation End-products’, or AGEs and also because of the harmful effects of too much insulinInsulin is a hormone made by the pancreas. It is responsible for making the body’s cells absorb glucose (sugar) from the blood…., the hormone that is released when your blood sugar levels goes high. Think of glucose, or blood sugar, as high-octane fuel. The goal of good nutrition is to deliver ‘slow-releasing’ carbohydrates that gradually break down into pure glucose fuel, which seeps into the bloodstream and is then escorted into cells to help keep your energy high. Too much glucose overloads brain cells, called neurons, which are less capable of dealing with the overload than muscle cells. This is called glucose neurotoxicity. ¹ This is backed up by studies that show higher blood glucose levels are associated with less functioning brain tissue in critical areas of the brain. ²

The hormone insulin escorts glucose into cells, either ensuring hungry cells get their due, or dumping excess glucose into storage. It’s a careful balancing act, and one that’s likely to go wrong if you keep eating sugary or refined carbohydrates. The more you eat these the higher your insulin levels and the more often you’ll have peaks in your blood sugar levels, followed by troughs. And this seesawing will leave you tired and unable to concentrate, eventually experiencing ‘blank-mind’ episodes and fading memory. Gradually your body will become less and less responsive to its own insulin – and develop ‘insulin resistance’. Someone in the grip of insulin resistance will produce more insulin in an attempt to get a response, a condition known as hyperinsulinemia, and get rebound blood sugar lows (hypoglycemia). Eventually, they will become so insulin resistant their blood sugar levels don’t go down as they should. Type 2 diabetes is the result.

The bitter truth about sugar

So, what’s all this got to do with preventing Alzheimer’s? The answer is everything. Being insulin resistant or diabetic, having hyperinsulinema or hypoglycemia, have all been shown to tremendously increase a person’s risk of developing Alzheimer’s or dementia.

There are probably many reasons why an upset in blood sugar control damages the brain, but one that stands out is the fact that occasional blood sugar peaks actually sugar-coat proteins, and damage them, creating damaged AGEs. A lifetime of sugar abuse, glycation (adverse interactions between glucose and proteins, for instance) and AGE creation lead to more and more artery and brain damage. The more the arteries become damaged, the worse the circulation to the brain and the less reliable the supply of nutrients becomes. So, ironically, eating too much sugar can lead to temporary glucose starvation to cells, as well as damage caused by excess glycation.

AGEs are not only bad for the brain – they also damage your skin, producing wrinkles and age spots. These damaged proteins produce 50 times the number of free radicalsFree radicals are molecules produced when the body breaks down food or by environmental exposure to things like cigarette smoke, pollution and radiation. Free radicals… that non-glycated proteins do, and promote inflammation in the brain as well as the skin, joints and other organs.

So oxidants and AGEs constitute a double whammy for your brain. Researchers now believe that AGEs may be a player in Alzheimer’s disease because they have been found in the neurofibrillary tangles that characterise the condition, and the formation of beta-amyloid plaque is significantly accelerated by the presence of AGEs.

The glucose/Alzheimer’s link

There has been much research into the links between blood sugar and Alzheimer’s. For example, researchers at Columbia University in New York studied 683 people without dementia who were 65 years or older for five and a half years. During that time, twice as many of the participants with high insulin levels developed dementia when compared to those with normal insulin levels. Also, the people with high insulin levels had the greatest decline in memory. ³ An Italian study of people free of dementia and diabetes showed that high insulin levels were strongly associated with poorer mental function. ⁴

Meanwhile, a six-year Swedish study of 1,301 people aged 75 and over showed that those with diabetes were one and a half times more likely to develop dementia. The risk was even greater in diabetics who also had high blood pressure or heart disease. ⁵ A number of other studies have also shown a strong association between diabetes and cognitive decline. ⁶

Having diabetes increases dementia risk by 20%. ⁷ Having a higher blood glucose (6.4 vs 5.5mmol/l) increases risk for dementia by 18 per cent. Diabetics with higher blood glucose levels (10.5 vz 8.9mmol/l) have a 40 per cent increased risk. ⁸

One of the best measures of your blood sugar control is something called glycated haemoglobinHaemoglobin is the protein that is found in red blood cells. It contains iron and is responsible for carrying oxygen from the lungs to the…. You want to have a score below 5.5 per cent. Researchers at the University of California, San Francisco, studied 1983 postmenopausal women and found those with glycosylated haemoglobin levels of 7 per cent or higher were four times more likely to develop mild cognitive impairment or dementia. ⁹

‘We suggest the term “Type 3 diabetes” to account for the underlying abnormalities associated with Alzheimer’s dementia-type of neurodegeneration,’ says Suzanna delaMonte in the European Journal of Neuropharmacology reviewing the evidence last year. ¹⁰

Why sugar is addictive

It’s one thing to know that sugar is bad for your brain, but another to quit eating it – especially when the desire for something sweet is one of the body’s strongest instincts. Your body and brain are much more responsive to deficiency than to having too much. There’s a simple reason for this. In evolutionary terms, starvation is a much more likely, and threatening, situation than today’s danger of excess. Consequently, we are all programmed to love sugar.

The way this programming works is that sugar causes the release of dopamineDopamine is a neurotransmitter (chemical messenger) found within the brain. It has a variety of influences on brain function including playing a role in regulating… and beta-endorphin, two neurotransmitters that make you feel good. So the more you have, the more you want, as you become less and less responsive to it. In short, you become addicted to it ¹¹ and no addiction is easy to break.

The late Dr Emanuel Cheraskin, Professor of Medicine at University of Alabama, calls sugar ‘the mother of all addiction’. ¹² Dr Candace Pert, Research Professor at Georgetown University Medical Center in Washington DC, says, ‘I consider sugar to be a drug, a highly purified plant product that can become addictive. Relying on an artificial form of glucose – sugar – to give us a quick pick-me-up is analogous to, if not as dangerous as, shooting up heroin.’ ¹³ Pert is one of the chief scientists involved in the discovery of the central role endorphins play in addiction.

If you are feeling depressed, especially in winter, there’s a good chance your brain levels of serotoninSerotonin is a hormone found naturally in the brain and digestive tract. It is often referred to as the ‘happy hormone’ as it influences mood…. are low. Serotonin is made from a constituent of proteinProteins are large molecules consisting of chains of amino acids. Proteins are essential nutrients for the human body – they are a building block of…, the amino acid tryptophan. However, ironically, eating a meal containing tryptophan doesn’t raise brain levels of tryptophan as high as eating a carbohydrateCarbohydrates are the primary source of energy for the body as they can be broken down into glucose (sugar) more readily than either protein or… meal does. This anomaly was discovered by Professor Richard Wurtman in a series of studies at Massachusetts Institute of Technology. He fed people standard American high-protein breakfasts versus high-carbohydrate breakfasts and found that only the latter boosted serotonin levels, despite containing no tryptophan! The reason for this is that tryptophan in the bloodstream competes very badly with all the other amino acidsAmino acids are commonly known as the building blocks of protein. There are 20 standard amino acids from which almost all proteins are made. Nine… in protein, so little gets across into the brain. However, when you eat a carbohydrate food such as a banana, this causes insulin to be released into the bloodstream – and insulin carries tryptophan into the brain.

This may be why depressed people instinctively crave sweet foods to give them a lift. So, if you find sugar improves your mood no end, you are probably low in serotonin. Having depression also increases dementia risk. Increasing the serotonin by supplementing 5-HTP and following a low GL diet are two proven ways to improve your mood in my book The Feel Good Factor. For more information on how to prevent Alzheimer’s read Alzheimer’s Prevention Plan.

Summary: say no to sugar and go for slow-release carbs

• Eat wholefoods – whole grains, lentils, beans, nuts, seeds, fresh fruit and vegetables – and avoid refined, white and overcooked foods.
• Eat five servings a day of dark green, leafy and root vegetables such as watercress, carrots, sweet potatoes, broccoli, Brussels sprouts, spinach, green beans or peppers, raw or lightly cooked.
• Eat three or more servings a day of fresh fruit, preferably apples, pears and berries.
• Eat four or more servings a day of whole grains such as rice, rye, oats, wholewheat, corn, quinoa, breads, pasta or pulses.
• Avoid any form of sugar or added sugar.
• Dilute fruit juices and only eat dried fruit infrequently in small quantities, preferably soaked or with a small handful of nuts or seeds.

REFERENCES

1. D Tomlinson and N Gardiner, Nature Neuroscience, Jan 2008
2. ME Mortby et al, PLoS ONE, Sept 2013
3. S Kalmijn et al, Ann Neurol, Nov 1997
4. E Hypponen and C Power, Am J Clin Nutr, Mar 2007
5. DJ Llewellyn et al, J Geriatr Psychiatry Neurol, Sep 2009
6. C Annweiler et al, J Alzheimer’s Dis, 2013 see also: KV Lu’o’ng and LT Nguyen, Am J Alzheimer’s Dis Other Demen, Mar 2013 see also; GK Pyapali et al J Neurophysiol, Apr 1998
7. W Katon, JAMA Psychiatry, Jun 2015
8. P Crane et al, N Engl J Med, Aug 2013
9. K Yaffe et al, J Nutr Health Aging, Jul-Aug 2006
10. S de la Monte, European Neurosychopharmacology, Dec 2014
11. SY Chung et al, J Nutr, Jun 1995 see also; M Cansev et al, Alzheimer’s Dement, Jan 2008 see also; M de Jesus Moreno, Clin Ther, Jan 2003 see also; MA Daniel et al, Nutrition, Nov-Dec 2003 (114-118) (can’t find 115)
12. SL Ladd et al, Clin Neuropharmacol, Dec 1993
13. DJ Canty and SH Zeisel, Nutr Rev, Oct 1992