What happens to your body with more carbohydrates consumption from processed foods?

What happens to your body with more carbohydrates consumption from processed foods?

If you are seeking health, having a healthy blood sugar level is a top priority. Many are busy with their works, forget their health and finally give time to illness. Happiness is nearly impossible with illness, lots of pain in the body. In our earlier article, we discussed how badly fructose sugar consumption can harm your body. Here is another sugar glucose. Here also we will explore What happens to your body with more carbohydrates consumption from processed foods? We will know why you need to take control of those simple carbohydrates from processed foods.

Sugar glucose comes from carbohydrates. But all carbohydrates are not the same. And that’s why the glycemic load of foods differs from each other. If you are eating more processed foods, you are likely to consume more glucose in the simple form. And if you don’t involve in vigorous physical activities you unlikely burn those calories. As a result, you will store them as fats. Not only storing as fat, but the consumption of such foods affects your health negatively in many ways.

What happens to your body with more carbohydrates consumption from processed foods?
Picture by Kidaha/Pixabay

A glimpse of types of carbohydrates

Carbohydrates are often classified according to the number of saccharide units they contain as monosaccharides, disaccharides, oligosaccharides, and polysaccharides. (1)

  • A monosaccharide contains a single saccharide or carbohydrate. E.g. Glucose(sugar from starch), fructose (sugar from fruits), Galactose (milk sugar)
  • A disaccharide gives two carbohydrate units such as sucrose(table sugar in common language), lactose (glucose and Galactose)
  • An oligosaccharide gives a “few” carbohydrate units, usually 3 to 10.
  • A polysaccharide gives many carbohydrates on hydrolysis, examples are starch and cellulose.

In common language, monosaccharides, disaccharides refer to simple sugar due to their simplicity in structure. Although we consume a variety of carbohydrates in different forms, the digestive system of the body finally breakdown it to the simple monosaccharides form as glucose, fructose, and galactose according to availability with the structure of particular carbohydrates. And here when we refer sugar we mean mainly glucose i.e. the simple form of carbohydrates and table sugar sucrose (a combination of fructose and glucose). We already discussed the numerous negative health effects of free fruit sugar consumption including weight gain and early aging in the previous article. In general, galactose comprises only a small part of a normal diet. And we are not talking about galactose here.

In thumb rule, processed foods and also some other foods like white rice, potato, raisins contain a simple form of carbohydrates in major and high Glycemic load. While your body takes time to break down, digest and absorb the complex carbohydrates, but need much lesser time to digest and absorb simple carbohydrates. As a result consumption of such simple carbohydrates suddenly release your blood sugar and calls insulin to rescue. More critically such foods don’t give satisfaction and you will feel hungry after a short time.

What happens to your body with more carbohydrates consumption from processed foods?

How your body use glucose?

When you eat glucose or carbohydrates, how your body uses them. Where they can go if you don’t use it as energy. How they are stored in your body? Let’s find. Almost every cell of your body uses glucose as energy. Glucose from carbohydrates is predominantly metabolized in cells of the body and about 20% of absorbed glucose is sent to the liver. (2) Carbohydrates or sugar from your food after breaking into simple sugar or glucose with exception of fiber, enter into the bloodstream from the intestine and circulates there. However, sugar can’t directly go from blood to cells or the liver for energy or store for future use. Here insulin acts like a key to absorb sugar from blood and deposits to cells. (3)

Insulin is a hormone produced by beta cells of the pancreatic islets that allows cells of skeletal muscle, liver and adipose tissue or fat cells to take up glucose from blood circulation. In tissue, it stores sugar or glucose either glycogen via glycogenesis or fats as triglycerides via lipogenesis, or in the liver store into both. (4, 5, 6) If you can’t remove blood glucose from your artery or blood vessel, it can cross the limits and inflames your artery and leads to serious conditions like organ failure. Therefore Insulin is a primary hormone that signals cells to lift glucose from the blood. (7)  

And finally, the absorbed excess carbohydrates in the form of glucose or simple sugar are converted into fats and stored in the liver, muscle, adipose, and several other tissues via insulin. (8)

Carbohydrates consumption from processed foods and weight gain or obesity

We have gone through that excess glucose when not used as energy, stored as fat in various tissues including adipose tissues. We have talked that glucose from carbohydrates converts to glycogen and fats when not use as energy. Glycogen is a form of immediate energy required for the case of an emergency. We have two major sources of glycogen as the liver and skeletal muscle. (9) And human has very limited capacity to store energy as glycogen approximately 15 g/kg body weight. If you are not an athlete or involved in similar activities and consuming large amounts of carbohydrates like glucose, then you are simply storing it as fats at various locations of your body as you are not burning them efficiently. (10,11,12)

However all carbohydrates are not the same, some are slow carbohydrates and some are fast. When you eat fast carbohydrates that are mostly refined and processed carbohydrates, your body will get suddenly too much energy. And if you are not burning those calories, your body will store as fat. On the other hand, whole foods like vegetables contain complex carbohydrates with fiber and vitamins and minerals take a longer time to digest and thus prevent the sudden release of sugar into the blood circulation and do the job in a controlled manner. (13) Researches evidenced the association of ultra-processed foods consumption with increased risk of obesity as well as metabolic syndrome, total and LDL cholesterol, and risk of hypertension. (14,15)

Study results

A 2019 Cross-sectional study in 19,363 Canadian adults of 18 years and more found that those who ate the most ultra-processed foods had 32% more tendency to be obese compared to those who ate the least. (16) Another 2019 published controlled clinical study conducted at NIH, researchers found an ultra-processed diet had increased calorie intake at an average of 508 calorie more per day and increased body weight 2 pounds or 0.9 kg on average just within 14 days in participants than those who consumed unprocessed foods. (17) And the list goes on.

Glucagon, glucose, insulin and fat store & burn

Glucagon a catabolic hormone secreted by alpha cells of the pancreas plays a major role in maintaining blood glucose level during fasting condition, exercise to prevent fall too low. It works just opposite to insulin. While metabolic hormone insulin participates in the removal of glucose from blood and store as fat, glucagon involves maintaining stable blood glucose levels from storage fats to burn as energy. For that glucagon acts in several ways

  • Glucagon takes part in the breakdown of fat stored in the liver in conversion to glucose and release to blood circulation via a process called glycogenolysis
  • It takes part in the production of energy i.e. glucose from amino acids through gluconeogenesis during prolonged fasting
  • Glucagon reduces the consumption of glucose by the liver to maintain blood glucose.

Although glucagon has the greatest effect on the liver, it also affects many different organs in the body, such as adipose tissue or fat cells, pancreas, brain, heart, kidney and some other tissues. (18) In summery glucagon promotes energy production from non-carbohydrate sources acting on fat cells, maintains blood glucose level for energy and inhibits the storage of carbohydrates as fats. Therefore you need proper regulation of these two opposite hormones. Deregulation of anyone affects the other. While low blood glucose, fasting, exercise, protein meal, stimulates glucagon secretion high blood glucose, dysfunction of the pancreas inhibits the process. (19)

High blood sugar, insulin suppress glucagon and thus prevent weight loss

High blood insulin is often associated with type 2 diabetes and most often caused by insulin resistance. (20) If you have insulin resistance, you also tend to have a higher blood glucose level. In healthy people low blood sugar trigger glucagon secretion, that converts stored fat into blood glucose for energy and restore normal blood glucose level. However, in diabetic people, high insulin showed inhibition in glucagon secretion. (21,22,23)

That’s why people with insulin resistance or high insulin, or type 2-diabetes find it hard to weight loss. Researchers concluded that weight loss itself as the strongest predictor of improved insulin sensitivity. (24) Your body’s primary objective is to keep you alive rather than fat loss. That’s why your body produces more insulin in response to high blood glucose to prevent organ failure.

Carbohydrates consumption from processed foods and Insulin Resistance

As we know the hormone insulin signals cells to lift sugar or glucose from your bloodstream to store or use. If you develop insulin resistance, your cells start resisting or ignoring the signal of insulin. Removal of excess sugar from your blood is a top priority of the body. And with the development of insulin resistance, the pancreas tries to remove sugar from the blood by producing more insulin. That increases the load on the insulin-producing beta cells of the pancreas. And a condition called prediabetic occurs when someone already has insulin resistance or pancreas aren’t making enough insulin to keep blood glucose in the normal range. (25)

Adipose tissue or fat cells and glucose consumption

Your adipose tissue composed mainly of fat cells are connective tissues that work for (26,27)

  • Storing energy in the form of fat for future use and release when required
  • Provide cushions to the body against shock
  • Insulates the body from external temperature.

But later research adipose tissue not only stores fat and sleep. As an endocrine organ with a complex network, adipose tissue participates in diverse biological functions including the production and secretion of several hormones. They can expand along with the size of fat cells with increased storage requirements. They help us by storing glucose and fat from blood circulation and thereby help you to maintain your blood below the toxic level. However, like most other things, fat cells have a saturation point at which they lose the capacity to store more lipids. At this point your fat cells become angry, dysfunction at fat cells occurs, they express stress signals. With the enlargement of adipose tissue, other metabolic problems begin to occur. (28, 29)

Enlarged fat cells, weight gain, chronic inflammation, and cell damage

And further calorie overloaded leads to fat accumulation in organ tissues such as liver, skeletal muscle, and heart and in other vital locations. Such a condition may interfere with the maintenance of an optimal state of health. That results in the release of toxic free radicals (30), commonly defined as “lipotoxicity. Such conditions lead to chronic inflammation and cells start to ignore the signals of insulin and develop insulin resistance and metabolic dysfunction. (31)

With chronic inflammation, numerous dysfunctions occur including cell damage. That’s why in today’s world minimizing chronic inflammation is the primary importance for better health. Enlarged fat cells promote inflammation and obesity itself is characterized by chronic low-grade inflammation. (32) And overweight or obesity is characterized by increases in fat cell number, fat cell size, or a combination of the two. The storage of fat occurs at adipose tissue and the liver occurs via Lipogenesis. While a high sugar diet stimulates this process with conversion into triglycerides in later, fasting and polyunsaturated fats inhibit lipogenesis. Hormone leptin also partly inhibits this process. (29)

Although polyunsaturated fats inhibit lipogenesis, you need to careful in selecting polyunsaturated fats. Due to the weak structural bonds, they can go rancid easily and become toxic. And the fasting glucose test is not a good indicator of insulin resistance. Being overweight or having obesity are risk factors for developing insulin resistance or prediabetes. (25)

Also, read 8 lesser-known foods that cause inflammation in your body  13 powerful anti-inflammatory foods but lesser-known to protect your health.

And how to choose the right cooking oil for the kitchen.

Carbohydrates consumption from processed foods and diabetes

We know the pancreas produces and secretes the hormone insulin in response to glucose and some protein-containing foods.

Know more about the Glycemic index, glycemic load & insulin index, why the differences matter?

When you have more glucose than the normal allowable limit and you are not able to remove glucose from your blood circulation, you are declared as diabetic.  In type 1-diabetes the beta cells of the pancreas unable to produce insulin efficiently. And scientists found the presence of both dysfunctions of the pancreas and peripheral insulin resistance in tissues in type 2-diabetes. (33)

We know that the body stores excess carbohydrates fat. And that excess sugar from carbohydrates also leads to high blood fat as triglyceride but low HDL. (34) Researchers demonstrated that the excessive influx of lipids due to high sugar consumption can reach the adipose tissue, the skeletal muscle, where it triggers insulin resistance or the pancreas. (35) With a recent study, researchers demonstrated that excess stimulates blood insulin levels precipitating “a self-reinforcing cycle” in which insulin stimulates fat production. A fatty liver also spills fats to other parts of the body. And overspill of fats into several tissues, including the pancreas clogs up the pancreas with fats which cause production and secretion insulin affectively and that cause type 2 diabetes. (36)

In addition consumption sugar including glucose, fructose and alcohol activate the formation of reactive free radicals. And uncontrollable amount with excessive consumption leads to an inflammatory response which can cause tissue damage. (35,37)

Carbohydrates consumption from processed foods and LDL subclass pattern

We learned earlier LDL as bad cholesterol and HDL as good cholesterol. Cholesterol is not that simple. LDL is further classified into larger LDL and small high-density LDL particles. (38) Research suggests that modified LDL particles such as oxidized, glycated, etc accumulate in the wall of the blood vessels, not other native LDL cholesterol. And that further leads to narrowing or blockage of the artery. And a blockage or narrowing artery or blood vessels leads to heart disease or stroke. Modified LDL also possesses pro-inflammatory properties and has the capability of damage further. (39)

Individual who have mostly small LDL particles, called Pattern B, and people with predominantly large particles, called Pattern A. And individual with pattern B has much higher up to the threefold increased risk of heart attack than pattern A. (40) Which may be due to factors like increased risk of oxidation and increased ability penetrate the wall of blood vessel and self-associate. (39,41) Studies suggest that small dense LDL can have multiple origins, at least in the individual with metabolic disorders with higher levels of triglyceride. (39,42) Scientists found an association of excess body weight and high-carbohydrate diets with increased concentrations of small, dense low-density lipoprotein (LDL) particles (pattern B). To the positive hope, in a clinical study researchers found cutting weight by reduced glucose consumption had led to change of Pattern B to Pattern A . (43)

And also the consumption of sugar-sweetened beverages for 2 weeks increased risk factors for cardiovascular disease with a drastic increase of triglycerides and apolipoprotein B. (44) Apolipoprotein B is involved in the metabolism of lipids and is the main protein constituent of lipoproteins such as very-low-density lipoprotein (VLDL) and LDL. (45) It is now widely accepted as the most important causal agent of heart disease. (46)

High blood sugar and heart disease

In glucose challenge study in normal people, researchers found glucose intake stimulates the generation of free radicals. And so increases oxidative load and causes a fall in protective vitamin E concentration in blood. (37) For that reason, too much sugar in your blood can lead to severe inflammation that results in organ failure. (47) This pro-inflammatory high blood sugar is a major cause of damage to blood vessels. (48)

And a damaged blood vessel further increases inflammation, oxidation of cholesterol results in fatty deposits in the wall of the blood vessel and narrowing artery. When such fatty deposits or plaque ruptures the body tries to repair it by sending platelets to seal it up. Due to small passage through a blood vessel, platelets could block the flow of blood to the heart or brain. When there is an interruption of oxygen-rich blood flow to heart or stroke, cells of that particular area of the heart or brain dies resulting in a heart attack or stroke. (49)

Also, read foods that reduce cholesterol naturally.

Moreover, if you have obesity you also have chronic low-grade inflammation in your body. (30) Diabetes has a well-established link with heart disease. (50) And researchers found both insulin resistance and obesity may become more prominent in promoting atherosclerosis or heart disease. (51)

Study findings on diabetes and heart disease

Data from the National Heart Association from 2012 shows 65% of people with diabetes will die from some sort of heart disease or stroke. The Framingham Study evidenced that people with diabetes are more vulnerable to heart disease than those people who did not have diabetes. Heart disease is an inflammatory disease with the oxidation of cholesterol.  High blood sugar increases the production of free radicals that tears sensitive cell components and inflames blood vessels. (52)

To make the situation worse, the incidence of metabolic diseases is also increasing with younger people. In Dec. 2019 published Review in the Journal of Nutrients, researchers found cardiometabolic disease symptoms typically observed in adults, such as hypertension, high blood glucose, abnormal blood cholesterol, and inflammation are becoming increasingly common in adolescents with obesity. (53)

In the blockage or narrowing artery, there is not only fatty cholesterol deposition, but there is also calcium deposition. Know why calcium and vitamin d can be disastrous without vitamin K. And you also need magnesium. Read more about magnesium for glucose control and cardiovascular health.

Also, read mitochondrial energy booster CoenzymeQ10 and about the amino acids the building block of cells that improves heart health and functions.

Carbohydrates from processed foods consumption, Diabetes, and Premature Aging

In our earlier article, we discussed the formation of Advanced glycation end products or AGEs. Excessive AGEs formation contributes to early aging. It can contribute to your skin wrinkled, sagging, dark circles under eyes, etc. Researchers found higher blood AGEs or Advanced glycation end products people with diabetes. (54,55)The release of nitric oxide inside the blood vessels moistens the inner lining of the blood vessels, smoothen blood flow and prevent fatty deposition inside the blood vessel. AGEs block nitric oxide activity in the endothelium and cause the production of reactive free radicals. (56) Also increased level of inflammatory AGEs in the blood is associated with damage to the inner lining of blood vessels and highlighting the progressively increased risk of vascular damage further leads to a heart attack. (57)

Carbohydrates from processed foods consumption and Cognitive impairment

We have already gone through that tissue wise chronic inflammation due to obesity and high blood glucose opens the path in the development of diseases like insulin resistance, diabetes mellitus, heart disease, metabolic syndrome and many more. (30) Such chronic inflammation, metabolic syndrome negatively impacts cognitive performance and brain structure with potential impairment of vascular reactivity, neuroinflammation, oxidative stress, and abnormal brain lipid metabolism. The brain region hippocampus is associated with cognitive functions like learning, memory, and mood. Researchers found volume losses in the hippocampus and frontal lobes in adolescents with metabolic syndrome. (58, 59)

Many studies found impairment of cognitive function with processed food consumption

Animal studies, as well as longitudinal studies, observed negative effects on the hippocampus with a processed foods diet. (60,61) In a clinical study researchers from the University of Wales from the UK examined the cognitive effects of simple processed and complex carbohydrates on 71 female students. After several hours of consumption, researchers found impaired cognitive behavior like a memory for hard words in students who had consumed simple processed carbohydrates. (62) Another clinical study on 21 participants with type 2 diabetes, researchers found, impaired cognitive functions like memory, attention, execution, etc in participants who had taken simple carbohydrates than those who take complex carbohydrates of the same amount. (63)

In a 2019 published study from the Radiological Society of North America, researchers found damage to brain regions using an MRI scan in obese teens probably due to inflammatory response. (64) Additionally a 2019 review, researchers also observed impairment of mental health such as increased level of stress, depression and reduced resilience in adolescents with obesity. (65)

Other diseases related to processed foods overconsumption

Not only above processed foods overconsumption, but damaged blood vessels can also lead to many health problems such as (66, 67)

  • Kidney disease or kidney failure
  • Vision loss or blindness
  • The weak immune system, with a greater risk of infections
  • Erectile dysfunction diminished sexual functions
  • Nerve damage that also causes tingling, pain, or less sensation in your feet, legs, and hands
  • Poor circulation to the legs and feet
  • Slow wound-healing  
  • Female infertility
  • Age-related macular degeneration

Apart from these American Society of Clinical Oncology suggests education and awareness as apart from other diseases like heart diseases and diabetes, obesity also plays a role as a contributor to cancer—in terms of both risk and mortality. From their data overweight and obesity are implicated in 15% to 20% of total cancer-related mortality. (68)

Also, read foods that help to reduce high blood pressure.

Bottom line

In conclusion processed consumption suddenly increases blood glucose, calls for a high level of insulin, stored as fat, results in chronic inflammation, cognitive impairment and puts your health in a number of risks. On the other hand, normally carbohydrates from whole foods differ from processed foods. Whole foods containing a good amount of fiber release glucose in the bloodstream in a controlled manner, don’t have the same effect as processed or refined foods.

Many don’t know what happens to the body with more carbohydrates consumption from processed foods? Some people know how those foods are killing their health and try to take it control. And many even don’t know why they are eating those comfort foods. They don’t know the existence of some factors that push them to eat processed foods, sugar-sweetened beverages. I have seen many who were struggling, many tried but failed in the long term. Foods that demand an enormous amount of willpower fail in the long term. We will explore the hidden sciences behind the consumption of such foods and the paths to beat such craving permanently.

Disclaimer: Information provided here are generalized information for  
informational and entertainment purpose only,  not intended to provide one  
to one health consultation or replace practice of a qualified practitioner.  
Different people may have different health condition and may have different  
reaction to the same food. Hence it has been advised to consult with health  
care provider before application of any of above information 
Source and references:
2. Schwarz J, Clearfield M, Mulligan K. Conversion of Sugar to Fat: Is  
Hepatic de Novo Lipogenesis Leading to Metabolic Syndrome and Associated  
Chronic Diseases?. J Am Osteopath Assoc 2017;117(8):520–527. doi: 
5.Flatt JP. Conversion of carbohydrate to fat in adipose tissue: an energy-
yielding and, therefore, self-limiting process. J Lipid Res. 
7. Asmat U, Abad K, Ismail K. Diabetes mellitus and oxidative stress-A 
concise review. Saudi Pharm J. 2016;24(5):547–553. 
9. Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H 
Freeman; 2002.  Chapter 21, Glycogen Metabolism. Available from: 
10. Acheson KJ, Schutz  Y, Bessard T, Anantharaman K, Flatt JP, Jéquier E. 
Glycogen storage  capacity and de novo lipogenesis during massive 
carbohydrate overfeeding  in man. Am J Clin Nutr. 1988;48(2):240–247. 
11. Murray B, Rosenbloom C. Fundamentals of glycogen metabolism for coaches 
and athletes. Nutr Rev. 2018;76(4):243–259. doi:10.1093/nutrit/nuy001 
12. Pereira RM, Botezelli JD, da Cruz Rodrigues KC, et al. Fructose  
Consumption in the Development of Obesity and the Effects of Different  
Protocols of Physical Exercise on the Hepatic Metabolism. Nutrients. 
2017;9(4):405. Published 2017 Apr 20. doi:10.3390/nu9040405
13. Monteiro, C., Cannon, G., Moubarac, J., Levy, R., Louzada, M., &  
Jaime, P. (2018). The UN Decade of Nutrition, the NOVA food  classification 
and the trouble with ultra-processing. Public Health Nutrition, 21(1), 5-
17. doi:10.1017/S1368980017000234 
15. Enes CC, Camargo CM, Justino MIC. Ultra-processed food consumption and 
obesity in adolescents. Rev Nutr. 2019;32:e18170. 
16. Nardocci M, Leclerc  BS, Louzada ML, Monteiro CA, Batal M, Moubarac JC. 
Consumption of  ultra-processed foods and obesity in Canada [published 
correction  appears in Can J Public Health. 2018 Oct 23;:]. Can J Public 
Health. 2019;110(1):4–14. doi:10.17269/s41997-018-0130-x 
18. Min KyunPark, Handbook of Hormones, Academic Press, Comparative 
Endocrinology for Basic and Clinical Research, 2016, Pages 129-131, e17A-2-
19. Rix I, Nexøe-Larsen C, Bergmann NC, et al. Glucagon Physiology. 
[Updated  2019 Jul 16]. In: Feingold KR, Anawalt B, Boyce A, et al., 
editors.  Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 
2000-.  Available from: https://www.ncbi.nlm.nih.gov/books/NBK279127/ 
21. Vergari, E., Knudsen, J.G., Ramracheya, R. et al. Insulin inhibits 
glucagon release by SGLT2-induced stimulation of somatostatin secretion.                     
Nat Commun 10, 139 (2019). https://doi.org/10.1038/s41467-018-08193-8
22. Kaneko K, Shirotani T, Araki E, et al. Insulin inhibits glucagon 
secretion by the activation of PI3-kinase in In-R1-G9 cells. Diabetes Res 
Clin Pract. 1999;44(2):83–92. doi:10.1016/s0168-8227(99)00021-2  
23. Godoy-Matos, A.F. The role of glucagon on type 2 diabetes at a glance.                     
Diabetol Metab Syndr 6, 91 (2014). https://doi.org/10.1186/1758-5996-6-91
24. Clamp LD, Hume DJ, Lambert EV, Kroff J. Enhanced insulin sensitivity in  
successful, long-term weight loss maintainers compared with matched  
controls with no weight loss history. Nutr Diabetes. 2017;7(6):e282. 
Published 2017 Jun 19. doi:10.1038/nutd.2017.31 
25.Insulin Resistance & Prediabetes, The National Institute of Diabetes and 
Digestive and Kidney Diseases Health Information Center, 
26. Birbrair A, Zhang T, Wang ZM, et al. Role of pericytes in skeletal 
muscle regeneration and fat accumulation. Stem Cells Dev. 2013;22(16):2298–
2314. doi:10.1089/scd.2012.0647 
28. Haczeyni F, Bell-Anderson KS, Farrell GC. Causes and mechanisms of 
adipocyte enlargement and adipose expansion. Obes Rev. 2018;19(3):406–420. 
29. Coelho M, Oliveira T, Fernandes R. Biochemistry of adipose tissue: an 
endocrine organ. Arch Med Sci. 2013;9(2):191–200. 
30.Ellulu MS, Patimah I, Khaza'ai H, Rahmat A, Abed Y. Obesity and 
inflammation: the linking mechanism and the complications. Arch Med Sci. 
2017;13(4):851–863. doi:10.5114/aoms.2016.58928
31. Sam S, Mazzone T. Adipose tissue changes in obesity and the impact on 
metabolic function. Transl Res. 2014;164(4):284–292. 
32.Andrew S Greenberg, Martin S Obin,  Obesity and the role of adipose 
tissue in inflammation and metabolism, The American Journal of Clinical 
Nutrition, Volume 83, Issue 2, February 2006, Pages 461S–465S, 
33.Dario Giugliano, Antonio Ceriello, Katherine Esposito,  Glucose 
metabolism and hyperglycemia, The American Journal of Clinical Nutrition, 
Volume 87, Issue 1, January 2008, Pages 217S–222S, 
34. Parhofer KG. Interaction between Glucose and Lipid Metabolism: More 
than Diabetic Dyslipidemia. Diabetes Metab J. 2015;39(5):353–362. 
35.Pereira RM, Botezelli JD, da Cruz Rodrigues KC, et al. Fructose  
Consumption in the Development of Obesity and the Effects of Different  
Protocols of Physical Exercise on the Hepatic Metabolism. Nutrients. 
2017;9(4):405. Published 2017 Apr 20. doi:10.3390/nu9040405
37. Mohanty P, Hamouda  W, Garg R, Aljada A, Ghanim H, Dandona P. Glucose 
challenge stimulates  reactive oxygen species (ROS) generation by 
leucocytes. J Clin Endocrinol Metab. 2000;85(8):2970–2973. 
38. Gardner CD, Fortmann SP, Krauss RM. Association of Small Low-Density  
Lipoprotein Particles With the Incidence of Coronary Artery Disease in  Men 
and Women. JAMA. 1996;276(11):875–881. doi:10.1001/jama.1996.03540110029028
39. Ivanova EA, Myasoedova VA, Melnichenko AA, Grechko AV, Orekhov AN. 
Small  Dense Low-Density Lipoprotein as Biomarker for Atherosclerotic  
Diseases. Oxid Med Cell Longev. 2017;2017:1273042. doi:10.1155/2017/1273042
40. Austin MA, Breslow JL, Hennekens CH, Buring JE, Willett WC, Krauss RM.  
Low-Density Lipoprotein Subclass Patterns and Risk of Myocardial  
Infarction. JAMA. 1988;260(13):1917–1921. 
41.Krauss RM. Heterogeneity of plasma low-density lipoproteins and 
atherosclerosis risk. Curr Opin Lipidol. 1994;5(5):339–349. 
42. Dreon DM, Fernstrom  HA, Williams PT, Krauss RM. LDL subclass patterns 
and lipoprotein  response to a low-fat, high-carbohydrate diet in women. 
Arterioscler Thromb Vasc Biol. 1997;17(4):707–714. 
43. Siri-Tarino PW, Williams PT, Fernstrom HS, Rawlings RS, Krauss RM.  
Reversal of small, dense LDL subclass phenotype by normalization of  
adiposity. Obesity (Silver Spring). 2009;17(9):1768–1775. 
44. Stanhope KL, Bremer  AA, Medici V, et al. Consumption of fructose and 
high fructose corn  syrup increase postprandial triglycerides, LDL-
cholesterol, and  apolipoprotein-B in young men and women. J Clin 
Endocrinol Metab. 2011;96(10):E1596–E1605. doi:10.1210/jc.2011-1251
46. Shapiro MD, Fazio S. Apolipoprotein B-containing lipoproteins and 
atherosclerotic cardiovascular disease. F1000Res. 2017;6:134. Published 
2017 Feb 13. doi:10.12688/f1000research.9845.1
48. Peiró C, Romacho T, Azcutia V, et al. Inflammation, glucose, and  
vascular cell damage: the role of the pentose phosphate pathway  [published 
correction appears in Cardiovasc Diabetol. 2017 Feb  16;16(1):25]. 
Cardiovasc Diabetol. 2016;15:82. Published 2016 Jun 1. doi:10.1186/s12933-
50. The Role of Inflammation in Diabetes: Current Concepts and Future 
Perspectives,European Cardiology Review 2019;14(1):50–9, 
51.  Averill MM, Bornfeldt KE. Lipids versus glucose in inflammation and 
the pathogenesis of macrovascular disease in diabetes. Curr Diab Rep. 
2009;9(1):18–25. doi:10.1007/s11892-009-0005-x  
52. University of Rochester Medical Center. "How Diabetes Drives  
Atherosclerosis." ScienceDaily. ScienceDaily, 17 March 2008.  
53. Ruiz LD, Zuelch ML,  Dimitratos SM, Scherr RE. Adolescent Obesity: Diet 
Quality,  Psychosocial Health, and Cardiometabolic Risk Factors. Nutrients. 
2019;12(1):E43. Published 2019 Dec 23. doi:10.3390/nu12010043 
54.Gkogkolou P, Böhm M. Advanced glycation end products: Key players in 
skin aging?. Dermatoendocrinol. 2012;4(3):259–270. doi:10.4161/derm.22028 
56.Alison Goldin,Joshua A. Beckman,Ann Marie Schmidt, and Mark A. Creager,
Advanced Glycation End Products, Sparking the Development of Diabetic 
Vascular Injury,  (2006). "American Heart Association". Circulation. 114 
(6): 597–605. doi:10.1161/CIRCULATIONAHA.106.621854. 
57.de la Cruz-Ares, S.; P. Cardelo, M.; M. Gutiérrez-Mariscal, F.; D.  
Torres-Peña, J.; García-Rios, A.; Katsiki, N.; M. Malagón, M.;  López-
Miranda, J.; Pérez-Martínez, P.; M. Yubero-Serrano, E. Endothelial  
Dysfunction and Advanced Glycation End Products in Patients with Newly  
Diagnosed Versus Established Diabetes: From the CORDIOPREV Study. Nutrients 
2020, 12, 238.  
58.Yates KF, Sweat V, Yau PL, Turchiano MM, Convit A. Impact of metabolic  
syndrome on cognition and brain: a selected review of the literature. 
Arterioscler Thromb Vasc Biol. 2012;32(9):2060–2067. 
59. Owen, L. and Corfe, B. orcid.org/0000-0003-0449-2228 (2017) The role of 
diet and nutrition on mental health and wellbeing. Proceedings of the 
Nutrition Society, 76 (4). pp. 425-426. ISSN 0029-6651, 
60.Calvo-Ochoa, E., Hernández-Ortega, K., Ferrera, P., Morimoto, S., and  
Arias, C. 2014. Short-term high-fat-and-fructose feeding produces  insulin 
signaling alterations, dendritic and synaptic loss and  astroglial response 
in the rat hippocampus. J. Cereb. Blood Flow Metab. 34:1001–8. doi: 
61.Tasnime Akbaraly, Claire Sexton,Eniko Zsoldos,Abda Mahmood,Nicola 
Filippini, Clarisse Kerleau,Jean-Michel Verdier, Marianna Virtanen, Audrey 
Gabelle, Klaus P. Ebmeier,Mika Kivimaki, Association of Long-Term Diet 
Quality withHippocampal Volume: Longitudinal Cohort Study, The American 
Journal of Medicine,  Volume 131, Issue 11, November 2018, Pages 1372-
62.Benton D, Ruffin  MP, Lassel T, et al. The delivery rate of dietary 
carbohydrates affects  cognitive performance in both rats and humans. 
Psychopharmacology (Berl). 2003;166(1):86–90. doi:10.1007/s00213-002-1334-5 
63.Papanikolaou Y,  Palmer H, Binns MA, Jenkins DJ, Greenwood CE. Better 
cognitive  performance following a low-glycaemic-index compared with a  
high-glycaemic-index carbohydrate meal in adults with type 2 diabetes. 
Diabetologia. 2006;49(5):855–862. doi:10.1007/s00125-006-0183-x 
64. Radiological Society of North America. "MRI reveals brain damage in  
obese teens." ScienceDaily. ScienceDaily, 25 November 2019.  
65.Ruiz LD, Zuelch ML, Dimitratos SM, Scherr RE. Adolescent Obesity: Diet  
Quality, Psychosocial Health, and Cardiometabolic Risk Factors. Nutrients. 
2019;12(1):E43. Published 2019 Dec 23. doi:10.3390/nu12010043
66. https://www.webmd.com/diabetes/how-sugar-affects-diabetes#2 
67. Giagulli, V.A.; Castellana, M.; Murro, I.; Pelusi, C.; Guastamacchia,  
E.; Triggiani, V.; De Pergola, G. The Role of Diet and Weight Loss in  
Improving Secondary Hypogonadism in Men with Obesity with or without  Type 
2 Diabetes Mellitus. Nutrients 2019, 11, 2975.
68.Ligibel JA, Alfano CM, Courneya KS, et al. American Society of Clinical 
Oncology position statement on obesity and cancer. J Clin Oncol. 
2014;32(31):3568–3574. doi:10.1200/JCO.2014.58.4680  
Bikramjit Konwar

Author: Bikramjit Konwar


2 Responses

  1. Appreciating the time and effort you put into your website and in depth information you present.
    It’s nice to come across a blog every once in a while that isn’t
    the same unwanted rehashed information. Great read!
    I’ve bookmarked your site and I’m adding your RSS feeds to
    my Google account.

Reaching Goal in Life-Yoga of Freedom

Social Media

Most Popular

Get The Latest Updates

Subscribe To The Updates

No spam, notifications only about new products, updates.


On Key

Related Posts

%d bloggers like this: