The blogger is pleased to post the following informative article (with express consent from the author) on the subject of “Sugars, Diabetes & Heart Diseases” from the Great Sifu Dr. JB Lim for the benefit of readers of this blog. Certain keywords are highlighted in red by the blogger to catch the eyes.
From: Lim Juboo
Date: Wed, Jun 25, 2014 at 9:18 PM
“Dear Dr Lim,
We like fruits and take a lot of fruits but my wife has started to avoid sweet fruits the last few years.
1. My question is: taking a less-ripe and thus less-sweet mango and taking a more-ripe and sweeter mango, will they give different reactions to blood sugar level? I thought all would turn into simple sugar and give the same surge in blood sugar level; one might be slower than the other.
2. Hope you could comment on the following. My wife is in her early 60s. Her parents were both diabetic when they were living. Her 2 elder brothers and 1 elder sister are diabetics, under control and become diabetic in the last few years. My wife's blood sugar is on the borderline and she is careful about carbo and sugar intake.
Thanks,
Hon”
Dear Ir. Hon,
You have asked two very good questions on sugars, diabetes, and family history of diabetes.
In order to answer that question, I need to break them into two sections:
1. One concerns food science and nutrition,
2. Genetics, molecular medicine and pathology (I shall deal with this later).
Your question can be very tricky, technical and lengthy to answer, as there is no simple ‘yes’ or ‘no’.
I shall try to make my answers as simple, and as short as possible because technical language in nutrition requires a good understanding on food chemistry, clinical and nutrition biochemistry, nutrition, pathology and medicine. They can be very lengthy and highly complex if it is to be explained properly in technical language.
So what I shall do is I shall try my level best to simplify my answer taken from numerous studies:
Food Science:
This depends. Let us take exactly two similar unripe fruits – one grown on the tree, the other plucked out from the tree and allowed to ripen on its own. Fruits that can ripen on their own after been harvested are called climacteric fruits.
Non-climacteric fruits can only ripen on the plant. Climacteric fruits have a short shelf life if harvested when they are ripe.
Let us say we take mangoes as an example. Mango is a climacteric fruit.
Let us assume we have mangoes A and B which have exactly the same weight and degree of ripeness on the tree. Let us now pluck mango A, and leave B alone to ripen on the tree.
Over a period of time, B will continue to grow further and gather more starch, fruit acids (citric, malic, tartaric, phytic, succinic, oxalic acids, etc) for conversion into sugars through photosynthesis.
A will be deprived of further nutrients, water and photosynthesis. Obviously A cannot grow any further. The starch within the fruit remains the same. This will ultimately be converted into fruit acids and sugars as it ripens on its own.
B being still on the tree will also undergo the same change except its energy (calories) greatly increases because of continuous water and nutrient supplies and through photosynthesis while still on the tree. Its sugar mixtures and acid/sugar ratios also change at different rates as it ripens.
In fruits (example mangoes in your case), whether climacteric or otherwise, the starch, sugars – disaccharides (sucrose) or monosaccharide (glucose and fructose) ratios varies from fruit-to-fruit, species-to-species, tree-to-tree, season-to-season…etc.
In all fruits including all types of mangoes, whether unripe or half ripe, they all contain starches initially. These are complex carbohydrates called polysaccharides. They are actually glucose units bond together. When hydrolyzed, or digested, all starches produced glucose as a simple sugar.
The half ripe mangoes contain a mixture of starches (polysaccharides), sucrose (glucose + fructose), glucose and fructose – the last two are simple sugars or monosaccharide.
The mixtures of starches and sugars vary tremendously from fruit-to-fruit, and also the degree of their ripeness varies.
Now the question is: what is the difference between these starches and sugars when they are finally converted into disaccharides and simple sugars (monosaccharide)?
One might think they are exactly the same because ultimately they are all burned off (metabolized) into carbon dioxide + water + energy once consumed by our body.
That is very true if our knowledge in biochemistry is only up to Form 6 Science. But this is not the case for a nutritionist who has to deal with the complexity of nutritional biochemical lesions and disease.
How then do these sugars affect her diabetic status and health? Before we answer that, let us understand a little chemistry about sugars.
What then are sugars?
Often when people talk about sugars they are often confused. Sugar is a kind of carbohydrate often referred to as mono- and disaccharides. Complex carbohydrate means polysaccharides such as starch.
Common disaccharides include, sucrose which is cane sugar or table sugar, and when hydrolyzed or digested, yields simple sugars (mono saccharides) called glucose + fructose. Sucrose is also found in sugar beets, honey, and corn syrup, whereas lactose (glucose + galactose) are found in milk and milk products. Other sugars like maltose which is a chemically a mixture of glucose+glucose, is derived from malt. Lactose is milk sugar, and is made from galactose and glucose units.
Galactose is a monosaccharide sugar and is less sweet than glucose and fructose.
The most common naturally occurring monosaccharide is fructose (found in fruits and vegetables). The term dextrose is the same glucose. In hospitals when a patient is put on an intravenous drip, it is usually saline + dextrose which mean it is a solution containing physiological (isotonic) saline + glucose.
Sugars that are found naturally in whole fruits, sweet potatoes, pumpkin or other vegetables is referred to as “intrinsic sugars”, whereas if you add sugar into them such as in syrups, soft drinks, beverages, fruit drinks or fruits canned in heavy syrups, then it is referred to as “extrinsic sugars” or added sugars.
Nutrition, Medicine and metabolism:
The metabolisms of sugars all take different pathways depending on whether it is glucose (grape sugar), fructose (fruit sugar), maltose (malt sugar), lactose (milk sugar). Let’s take just two examples – fruit sugar (fructose) and grape sugar (glucose).
Fructose:
Fructose or fruit sugar is found in most plants, fruits and vegetables. What happens if we eat them? Do they cause diabetes?
Fructose, or fruit sugar, is a simple ketonic monosaccharide (meaning it yields ketones bodies), and they are found in many plants. The fructose is often bonded to glucose to form the sucrose which is a disaccharide. Fruit sugar is a three monosaccharides combination, and along with glucose and galactose (milk sugar) that are absorbed directly into the bloodstream during digestion.
Unlike glucose, fructose does not require insulin to control its levels in the blood. On absorption, it goes straight to the liver. It is the glucose not fructose that causes harm in diabetic patients. Measurement of blood sugar always refer to glucose, and in glucose tolerance test it is always glucose (much less sweet) that the patient is given to drink before the test, not fructose (even though it is the sweetest) as it is not regulated by insulin.
The Metabolism of Fructose and health:
The evidences we have on the role of fructose on human health are not very clear. Although there are existing data to support metabolic and endocrine effects of dietary fructose that suggest that an increase in consumption of fructose may be detrimental in terms of body weight and adiposity, and that its metabolic indexes are linked to insulin resistance syndrome, much more studies are needed to fully understand the metabolic translation of dietary fructose in human nutrition.
This is partly because the sugar (fructose) takes a different metabolic pathway from that of glucose. It does this by bypassing the phosphofructokinase regulatory step directly into glycogen. Glucose or dextrose (grape sugar) can also be converted to glycogen rather than entering the glycolytic pathway.
As a consequence, fructose increases hepatic pyruvate and lactic acid production, triggers off pyruvate dehydrogenase, and swings the balance from oxidation to esterification of fatty acids
This then increases very-low-density lipoprotein synthesis which studies have shown bad for the heart.
In human feeding trials, fructose has had contradictory effects on plasma triglyceride levels, which may be correlated to factors such as the amount of fructose consumed; energy equilibrium, baseline triglyceride, insulin levels and glucose concentration.
Effect of a meal of fruit sugar:
The postprandial (after a meal) rise in triglyceride levels after fat intake may be amplified with the addition of fructose to a test meal. So it is a compounded effect.
Nevertheless, a study in individuals with type 2 diabetes demonstrated a lack of significant variation in glucose, lipid, and insulin responses to three 28-day isocaloric (equal energy content) feeding phase when 20% of calories were either fructose, sucrose, or starch.
Most of the carbohydrates in foods are made up of chains of glucose. When glucose enters the bloodstream, the body releases insulin to help regulate it. Insulin does not regulate fructose. Fructose is metabolized in the liver. The biochemistry to explain this is very complex, even though it is best explained in a highly technical biochemical language.
However, to make it exceeding simple to understand, we can say that when large amounts of fructose from ripe mangoes or any sweet fruits is eaten, it goes directly to the liver. The liver cannot cope with the flood of fructose.
It then changes all those fructose into triglycerides (fatty acids) and into fats.
Lipid Synthesis from Fructose:
Hence fructose though may not be responsible in inducing diabetes, or make it worse, can make a person obese and causes coronary heart disease. This is the same scenario link as a diabetic who is also prone to getting heart disease.
In short, all sugars in excess are bad for health, be they from honey, cane sugar, beet sugar, fruits, starches or from barley and malt.
When too much fructose enters the liver, the liver can't process it all fast enough for the body to use as sugar. Instead, it starts making fats from the fructose and sending them off into the bloodstream as triglycerides.
To explain further in slightly more sophisticated language of nutritional biochemistry, plasma insulin that regulates glucose and leptin (hormone that control satiety) act in the central nervous system in the long-term decree of energy homeostasis.
Since fructose does not stimulate insulin secretion from the beta cells of the pancreas, the consumption of fruits (including mangoes), and all foods or drinks containing fructose, generates smaller postprandial (after meal) insulin excretion than does consumption of glucose-enriched carbohydrate.
Since leptin production is controlled by insulin responses to meals, fructose consumption also decreases circulating leptin concentration.
The united effects of reduced circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the chances of weight gain and its linked metabolic sequelae.
Furthermore, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. This increases the blood triglyceride levels which then place the heart at risk to cardiac ischemic events.
In short, fructose consumption stimulates insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal studies.
Can fructose challenge insulin?
No it cannot. Fructose is not a scretagogue for insulin production (meaning it cannot stimulate insulin). Only glucose is an insulin stimulant. In fact some studies have shown it does the opposite by lowering insulin which is not good for those challenged with diabetes.
By a process called fructolysis almost all the fructose in fruits is metabolized exclusively and almost completely by the liver and converted and stored mainly (30 – 50 %) as glycogen and a smaller amount (1 %) is converted into trigycerides (fatty acids) or lactate (25 %).
Most of the enzymes used in the metabolisms of glucose and fructose via glycolysis are the same even though their metabolic pathways are different.
Finally, both glucose and fructose can be converted into glycogen in the liver and are used up for energy. However, fructose is not immediately available to the general body as a source of energy except by the liver, intestines, skeletal muscles, kidney, testis, brain, and fat tissues through transporters (carriers) primarily by GLUTS 5.
In other words, fructose can be converted into glucose via an enzyme called glycogen phosphorylase within about 8 -13 hours after a meal and used as a fuel. So this can also be a challenge to those compromised by diabetes.
However, another hormone called glucagon (produced by the pancreas) can counter signal to insulin to increase its production to kick up glycogenolysis and gluconeogenesis pathways to stabilize glucose equilibrium in the blood. So it can also act in the opposite pathway.
A large intake of dietary fructose also can speedily induce insulin resistance, postprandial hypertriglyceridemia (excessive fatty acids) and elevated blood pressure in humans more than starch (or glucose)
Additionally, it is an impending risk factor for fatty liver disease, metabolic syndrome, abdominal obesity, inflammation, oxidative stress, endothelial dysfunction, micro vascular disease, glomerular hypertension, fatty liver, and renal injury.
Hence the risks of these are potentially there if too much of fructose from very sweet mangoes or any food is taken at one sitting or habitually consumed even though it does not initially raise blood glucose levels.
Although fructose is not an immediate challenge to the insulin in diabetic patients, it is still a threat if large amounts of fructose in mangoes or from other food sources (example, from table sugar = glucose + fructose) are taken.
Hence we can see why fructose has the lowest glycemic index (extent it can raise blood sugar levels) of 19 compared to glucose which is 100. Yet fructose is the sweetest of all – some 1.7 times sweeter than ordinary sugar (sucrose). Just as we say ‘do not judge a book by its cover’ so can we say ‘do not judge a sugar by its sweetness’?
It may be so much less sweet, but it is most deadly – “pure, white and deadly” as the late Prof. Dr John Yudkin, Chair of Nutrition, University of London who found that sugar was the main cause of heart disease.
His findings rocked the entire medical and nutrition community throughout the world in the mid-1960s. John Yudkin a Jewish professor was a very eminent University of London physician, scientist and nutritionist who held the Chair of Nutrition at Queen Elizabeth College, London. He taught me when I was a postgraduate student there.
It is not cholesterol, brain, eggs, liver or any cholesterol-laden foods, but it is the pure white and refined sugar that is the main cause of heart disease.
I repeat. It is sugar, not cholesterol that is the main cause of ischemic heart disease. This is my personal advice to everybody, including members of the nutrition, dietetics, and medical community.
The Devil or the deep blue sea
So consuming too much sugar or too much sweet fruits put us in either the devil (diabetes), or in the deep blue sea (heart disease).
Glucose:
Let us now take the case of glucose which is the sole sugar that is responsible for diabetes, and the only sugar that is insulin-responsive.
The metabolism of glucose to produce energy is a highly complex equation. Let me try my best to simplify and drastically cut-short its complex metabolic mechanism.
We shall do this in just 3 steps, leaving out the numerous intermediary steps.
1. Glycolysis: the oxidative metabolism of glucose molecules to obtain adenosine triphosphate (ATP) which is a nucleoside triphosphate and into pyruvate.
2. The pyruvate from glycolysis then enters the Krebs cycle (Hans Kreb or Citric Acid Cycle) in a mammalian aerobic system (requires oxygen in its final stage to burn off as water, carbon dioxide + energy). In an anerobic (oxygen-free respiratory systems) organisms this is achieved after moving through pyruvate dehydrogenase complex.
3. The pentose phosphate pathway, which acts in converting hexoses into pentoses and in NADPH (nicotinamide adenine dinucleotide phosphate-oxidase) regeneration. NADPH is a crucial cellular antioxidant which blocks oxidative damage and acts as precursor for production of many other biomolecules.
The pentose phosphate pathway (phosphogluconate pathway and the hexose monophosphate shunt) is a biochemical route that generates NADPH and pentoses – a 5-carbon sugar. There are two distinct biochemical segments in this metabolic pathway.
The first is what we call, the oxidative phase, in which NADPH is generated, and the second is the non-oxidative synthesis of 5-carbon sugars. This is pathway where glucose takes as an alternative to glycolysis.
While it does involve oxidation of glucose, its key role is anabolic rather than catabolic. This is as far as glucose is concerned. Glucose is the only a simple example.
The level of circulatory glucose is the most important signal to the insulin-producing cells of the pancreas. The height of circulatory glucose is largely determined by the load-intake of dietary carbohydrates via insulin. In humans, insulin is secreted by beta cells in the pancreas.
Fat is stored in adipose tissue cells, glycogen in both - stored and released as needed by the cells of the liver.
Not considering the insulin levels, no glucose is released to the blood from internal glycogen stores from muscle cells.
These examples clearly show that simple sugars all take metabolic routes once they are absorbed into the blood stream, and they can cause different diseases later in life.
This is worse if there is a faulty gene somewhere in the chromosome leading to various enzyme deficiencies that impairs the metabolisms of various types of sugars. For instance, diabetes Type 1 may be caused by a defect in one of the genes. Let us not go into molecular medicine for the moment. I shall explain this separately in another article. But let us go into other examples.
Lactose:
Lactose (milk sugar) is the least sweet of all sugars. But it has its problems too for those with lactase deficiency.
Lactose intolerance from milk is found mainly in Asians who are unable to tolerate milk due to a deficiency in lactase in the small intestine. This is an enzyme that catalyzes lactose into glucose and galactose. Patients normally are presented with diarrhea, tummy upset and cramps.
The milk sugar (lactose) can be broken down into lactic acid and water by some of the bacteria - Lactobacillus delbrueckii subspbulgaricus and other lactobacilli in yogurt bacteria. Thus, if yogurt is taken at the same time, this can lessen the symptoms of milk intolerance who are sensitive to lactose.
Glycemic index or G. load?
Pure glucose is has a glycemic index of 100, and is used as the reference scale around which all other foods are gauged for their glycemic index.
For instance, a food with a glycemic index of 98 raises blood sugar almost as high as pure glucose, whereas, a food with a glycemic index of 10, raises blood sugar just by 1/10 as compared to pure glucose.
However in the practice of nutrition, dietetic or medicine, it is important to keep in mind that the glycemic index is the measure of a single food item. It does not take portion size into consideration. The fact is: it is the amount of food consumed that causes a rise in blood sugar level, not the glycemic index.
In short, it is how much you eat in one sitting that determines how sharply your sugar is going to rise postprandial. It takes into account the amount of food as well as the glycemic index. We call this glycemic load, and not just its glycemic index.
For instance, if you give just one sweet, or a very small slice of very sweet mango, or just 1 gram of glucose to a patient who is severely diabetic, it is not going to make an iota of difference to his blood sugar level. It is how much you give him that counts.
Remember also all sugars in excess are detrimental to health, be they glucose, fructose, lactose or galactose.
Hereditary deficit and sugar metabolic errors:
There are hereditary inborn errors of metabolism due to deficiencies in certain enzymes. That is even worse than Type 1 diabetes mellitus in adults.
For instance, hereditary fructose intolerance (HFI) is an inborn error of fructose metabolism. It is rooted by a deficiency of the enzyme aldolase B.
Individuals afflicted by HFI remain asymptomatic until they consume fructose, sucrose, or sorbitol.
If fructose is ingested, the enzymatic block at aldolase B triggers an accumulation of fructose-1-phosphate. This buildup has downstream effects on gluconeogenesis and regeneration of adenosine triphosphate (ATP).
The patient with HFI may be presented with vomiting, hypoglycemia, jaundice, hemorrhage, hepatomegaly (enlarged liver), hyperuricemia (high uric acid), and potential renal failure.
Death in HFI is always associated with misdiagnosis even by specialist clinicians not trained or familiar with genetic errors in metabolic diseases and nutrition.
Galactosaemia
This is another example how another sugar can harm for individuals who are intolerant. This is a rare genetic metabolic disorder that affects an individual's ability to metabolize galactose (milk sugar) properly. It is caused by an autosomal recessive mode of inheritance that confers a deficiency in an enzyme accountable for adequate galactose degradation.
Sugars are bad for health:
Remember also all sugars in excess are detrimental to health, be they glucose, fructose, lactose or galactose. They all are some of the root causes of diabetes, and heart disease as shown by Prof John Yudkin way back in the mid-1960s. Sugars are also linked to cancers, and a host of degenerative diseases from retinopathy in the eyes, cardiovascular events including CVA (stroke), to nephropathy (renal disorders)…etc
It is not possible for reasons I have given at the very beginning, whether or not it is an unripe, half ripe or a very ripe mango is injurious to a diabetic.
It depends on the mixtures of sugars – sucrose, glucose and fructose in them, and also the amount (load), and this depends on the species and their degree of maturity the fruit.
There are a lot of protective phyto-chemicals and antioxidants in fruits and vegetable too which I have to leave out, not considered in my simple answer.
Nutrition and health:
Whether it is consumption of mangoes, raw, half-ripe, or climacterically very ripe, or any other foods that is protective, or injurious to genetically predisposed diabetic individuals, nutrition is the single most important determinant to the causation of a variety of disease and disease prevention.
Genes and Nutrition:
The field of nutrigenomics (a specialized area in nutrition called nutritional genomics where scientists and research doctors study the effects of foods and nutrient principles on gene expression), and how they affect the genome of the individual; either by up-regulating or down-regulating the expression of certain genes and its sequel on the integral constitutional make-up of an individual towards disease prevention, or their future expression on pathogenesis and their outcome. These are issue in the domain of molecular nutrition and sequel pathologies.
Your question and my summary:
Whether it is raw, half ripe or very sweet and ripe mangoes (or any other fruits), they all contain a mixtures of carbohydrates, including starches, sucrose, fructose and glucose. All of them take different pathways, and affect the body differently:
Raw and half ripe mangoes have a lot of starch in them, and when starches are digested yields mainly glucose which is the only simple sugar that causes diabetes. So avoid large intake of half ripe mangoes to prevent a flood of glucose streaming into the blood. It is the glycemic load (total amount of glucose) that counts, and not the glycemic index.
Fructose has its own problem when the fruit is very ripe and sweet. It causes obesity and a rise in blood lipids. Hence this causes heart disease.
Sucrose which is a mixture of glucose and fructose when digested it is even worse. It aggravates blood sugar levels in diabetic, and has a fairly high glycemic index (60 -70). The glucose is contraindicated for those with diabetes, and the other devil is fructose that causes coronary heart disease. Sucrose has the greatest share of being a devil and the deep blue sea simultaneously.
The gold standard in nutritional practices is to eat a variety of foods in moderation, in small feeds, and not indulge in a gala eating of mangoes or any food at one sitting.
This should answer your first question. But I shall not tell you yes, or no. You answer this yourself as I have explained enough.
Post note:
Sorry for not giving you a straight forward ‘yes’ or ‘no’ answer. This is because I follow my Jewish professors’ footsteps who were my mentors in London and at Cambridge.
They would never give us students a straight forward reply that only requires a ‘yes’ or ‘no’.
Instead, they would give us a very lengthy one hour lecture every time and leave us very frustrated at the end to decide on our own whether it is a ‘yes or no’ answer.
That is the gold standard of British universities – critical and analytical thinking – and not spoon feeding education. So I am academically trained to follow their Jewish footsteps.
The Jews win 80 % of all the Nobel Prizes from Science, Medicine, Economic, and Peace to Literature, especially in America and the United Kingdom. They are such an intelligent, learned and unbeatable race.
I shall write a little on molecular medicine, gene expression and diabetes mellitus Type 1 and Type 2, family history of diabetes later in another article. Give me a little rest for the moment.
By lim juboo from Minyak Beku
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The blogger is grateful to have received the following feedback from Dr. Lim on the above posting and wishes to share respectfully with visitors of this blog:
Saturday, 28 June, 2014 6:30 PM
From: Lim Juboo
Dear Ir Sifu Lau,
I have quoted your website on sugars into my blog so that readers can go to yours instead. Mine is too dull and boring for visitors.
http://taionn.blogspot.com/2014/06/sugars-diabetes-heart-diseases-by-dr-jb_273.html in http://scientificlogic.blogspot.com/
You are really very good with illustrations, so artistically touched up even though you are an engineer. I do not know where you get all those pictures, photos and graphic; to the extent you even managed to get a picture of my professor - Professor Dr John Yudkin who was one of my professors at the University of London.
Professor Yudkin was such an eminent Cambridge-trained physician, physiologist, nutritionist and scientist combined; acknowledged world-wide, who taught us a lot of things about nutrition, medicine and clinical-nutritional biochemistry. He could explain very highly complex subject in a very simple way that it was just a joy to hear him lecture, especially with his hundreds of very rich clinically slides, photos (like yours), clinical features and presentations - case studies, statistics and so on.
My family and I visited him again at his apartment in up-class St John Wood in London in November 1993 when I took my family on a one month tour of Europe and the British Isle. He was such a kind and loving gentleman to all my young children even though he had aged so much by then. He passed away a few years later leaving a legacy behind him to the medical-scientific community. It was he, and another professor from Cambridge who was also one of our External Examiners who helped me admission into the Royal Society of Medicine as a Fellow in London after I got my PhD.
I have counter comment your rather flattery comment in my blog - crediting it to you.
regards
lim juboo