BASICS
- Glucose is a fast acting appetite suppressant.
- Fructose is a prolonged appetite stimulant.
- We often feel hungry when we are actually thirsty – fill up on water.
IDEAS
It is really simple. The glucose half of sugar tells that you have had enough and the fructose half makes you hungry for the next day.
That is the chemical reaction that is meant to keep you, the hunter gatherer, under that fruit tree at the end of summer, gorging away to make fat for winter hibernation.
I used to think that I had no willpower when it came to food but now I understand that it is a chemical called Fructose that is influencing my entire hunger mechanisms. With that knowledge comes control.
You can still have some sugar in your diet as long as you know what it is actually doing to you for the next couple of days afterwards. The big problem with society is the massive amount that we are having it three times a day, 365 days a year which starts from almost the time we are weaned off breast milk.
MORE INFORMATION
Glucose Effects
- Stimulates a release of Insulin from the pancreas which helps body tissues take up Glucose
- Insulin effect on the hypothalamus as an appetite suppressant.
Fructose Effects
Production of Free Fatty Acids in the liver that:
- Inhibits the Insulin effect on the hypothalamus and all tissues (Insulin resistance).
- Inhibits the Leptin (that was released from fat stores) effect on the hypothalamus.
- Stimulate the Ghrelin release from the stomach (which gives you the grumbling stomach).
Read more about Metabolism
Practical Principles
Once you exclude fructose then EAT ONLY WHEN YOU ARE HUNGRY and eat only until you have had enough to be satisfied.
You still need to watch the overall calories (kilojoules-kJ) taken in but now you will not be taking in the unnecessary ones. Try www.myfitnesspal.com or phone app Myfitnesspal – both free and easy to use. Otherwise get a calorie counter book.
Have the majority of your calories at the beginning of each day – then you can burn them off. Have a good breakfast, lighter lunch, and very light dinner.
Next time you’re hungry, have a large glass of water. A lot of times when you are thirsty, the brain registers that as hunger.
A large glass of WATER 30 minutes before each meal will distend the stomach so you will feel less hungry by the actual meal time.
Having a GLASS OF MILK at the same time will give you enough glucose to kick in the insulin effect, even before you start the meal. It also has a fat and protein load.
Chew each mouthful – take your time to eat. It also makes you less hungry.
Do you have a lack of willpower or is a chemical controlling you?
Our attraction for sweet food is a primitive and basic survival instinct. That is why the thought, vision and smell of sweet substances triggers a response in our nucleus accumbens, or addiction centre of the brain. We are meant to be addicted to the sweet taste as it is associated with a known food source of Fructose.
It all comes back to being a hunter gather from a metabolic aspect.
We are designed to search for sweetness because the Fructose that we are able to take on at times of plenty is metabolised to fat for the leaner periods and winter hibernation.
Just as we are designed to eat animals, we are meant also to graze on seeds, nuts and over the last several thousand years we have taken on the design to have milk and dairy products from our farming and domestication of animals.
Numerous people tell me that they find giving up sugar is harder than any other addiction. It appears to be certainly harder than giving up smoking.
However it is more about curbing that craving and being aware that when you are approaching a sweet substance that it is actually a chemical having its effect upon you rather than you having a lack of willpower.
2 Phases of Sugar Withdrawal
The first is about substituting something for the sweetness. That is when you can use other sweeteners. Ideally Glucose (from chemists) or Dextrose (brewers shops). These are really just Glucose and not as sweet as sugar. It is fine to use fruit with its higher fibre content to come down slowly.
It is probably okay to have some artificial sweeteners in this transition – diet soft drinks, cordials and lollies but I am NOT going to recommend it long term or in large amounts.
The second phase involves just going without that ‘sweet’ requirement. I gain the impression that may take 6 to 12 months, so don’t panic when the urge is still there. You just get used to cooking and eating without sweeteners. Vegetables, milk and even nuts taste sweet and food becomes tastier.
That longstanding sweetness of sugar has been dampening your taste for years.
When you start recognising the appetite stimulant and the addictive nature of this “natural” substance, then it is far easier to manage.
Stop seeing sweet food as a staple diet. Consider it at the very most as treats and certainly understand that they are just chemicals affecting your appetite and food intake control.
Contribute more to NoFructose.com
ARTICLES
Effects of Fructose vs Glucose on Regional Cerebral Blood Flow in Brain Regions Involved With Appetite and Reward Pathways
Kathleen A. Page, MD; Owen Chan, PhD; Jagriti Arora, MS; Renata Belfort-DeAguiar, MD, PhD; James Dzuira, PhD; Brian Roehmholdt, MD, PhD; Gary W. Cline, PhD; Sarita Naik, MD; Rajita Sinha, PhD; R. Todd Constable, PhD; Robert S. Sherwin, MD
JAMA. 2013;309(1):63-70. doi:10.1001/jama.2012.116975
‘In a series of exploratory analyses, consumption of fructose compared with glucose resulted in a distinct pattern of regional CBF and a smaller increase in systemic glucose, insulin, and glucagon-like polypeptide 1 levels.’
______________________________
Fructose ingestion and cerebral, metabolic, and satiety responses.
Purnell JQ, Fair DA.
JAMA. 2013 Jan 2;309(1):85-6. doi: 10.1001/jama.2012.190505.
‘when the human brain is exposed to fructose, neurobiologic al pathways involved in appetite regulation are modulated, thereby promoting increased food intake.’
_______________________________
Leptin and the Central Nervous System Control of Glucose Metabolism
The regulation of body fat stores and blood glucose levels is critical for survival. This review highlights growing evidence that leptin action in the central nervous system plays a key role in both processes. Investigation into underlying mechanisms has begun to clarify the physiological role of leptin in the control of glucose metabolism and raises interesting new possibilities for the treatment of diabetes and related disorders.
________________________________
2002 American Society for Clinical Nutrition
Fructose, weight gain, and the insulin resistance syndrome
Sharon S Elliott,et al
http://ajcn.nutrition.org/content/76/5/911.full
This review explores whether fructose consumption might be a contributing factor to the development of obesity and the accompanying metabolic abnormalities observed in the insulin resistance syndrome. The per capita disappearance data for fructose from the combined consumption of sucrose and high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997. Both plasma insulin and leptin act in the central nervous system in the long-term regulation of energy homeostasis. Because fructose does not stimulate insulin secretion from pancreatic β cells, the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose-containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae. In addition, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal models. The data in humans are less clear. Although there are existing data on the metabolic and endocrine effects of dietary fructose that suggest that increased consumption of fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome, much more research is needed to fully understand the metabolic effect of dietary fructose in humans.
More to follow