Sucrose is the primary source of modern disease

[RealNeat]

I'm not following, you seem to bring up a non-essential monosaturated fatty acid, while I was referring to omega-3 fatty acids. Are you implying that consumption or synthesis of oleic acid somehow compensates for every other fatty acid required in the body for optimal health? In which case, that couldn't be further from the truth.

I have not ignored Peats work, and I don't take everything for granted. I also like to do my own work, this is Peat-free subforum to discuss all types of literature in case you had forgotten.

Read what I wrote again. You practically can't be PUFA free, and of the natural foods one eats they get enough of the so called essential fats that there is no legitimate reason to take more, not because of some inefficiency of converting ALA or because there is some magical ratio of 3 to 6 If there is a need for a partially unsaturated fat oleic acid will be produced by the body to meet it's need. Your appeal to nature can be dissected in a million ways but suffice it to say that if sucrose alone was a driver of disease the fruits with the most sugar would be seen to cause disease, after all the offending compound is copious and a majority of what the fruit is comprised of (besides water). Yet we see over and over again that fruit intake is shown to be protective in almost every scenario. If sugar was so horrible we would not see fruit be of benefit, the micro and so called macro nutrients are not so plentiful that they offset the amount of sugar. Sugar in the diet can be of harm if sugar IS your diet. But most make sugar a part of their diet, it in no way has the harm that PUFA does in small quantities and to say it's a driver of disease is dishonest and poorly thought out.

 

[ThinPicking]

Roles of Glucose and Sucrose Intakes on the Brain Functions Measured by the Working Ability and Morris Maze

Sugars such as glucose or sucrose are considered hazardous foods because their intakes lead to obesity, further causing diabetes mellitus (DM), or cardiovascular diseases. However, glucose is needed for many brain functions such as memory and emotion among others. Glucose induces the secretion...

dx.doi.org

 

[RealNeat]

View attachment 59581

Roles of Glucose and Sucrose Intakes on the Brain Functions Measured by the Working Ability and Morris Maze

Sugars such as glucose or sucrose are considered hazardous foods because their intakes lead to obesity, further causing diabetes mellitus (DM), or cardiovascular diseases. However, glucose is needed for many brain functions such as memory and emotion among others. Glucose induces the secretion...

dx.doi.org

Ah ok I see what we are dealing with now. Figured.

Forum supporting doesn't make one immune to shilling, beware all who read and sway.

 

[Alpha]

Regarding purified sugar - as @youngsinatra said - it is only bad when the body cannot convert it into energy due to deficiencies. Also if the energy production mechanisms are somehow not working properly due to other reasons and the electrons are being leached and turned into fat/inflammation.

By itself sugar cannot cause damage if the organism is in a perfect state. Having said that - most are us are damaged already. But cutting out sugar/fruit is just a band-aid.

The body cannot convert sugar to energy on the spot, or oxidize it for energy, rather the liver prefers to turn it into fatty acids, then estrify it to triglycerides for transport on apolipoprotein B-100 along with cholesterol for storage. Particularly it is fructose, or worse, the combination of fructose and glucose in a short a amount of time that leads to rapid energy conservation rather than energy liberation. The amount of people who have vitamin or mineral deficiencies to disrupt the ATP or oxidation process is almost non-existent, rather it is a biochemical process exacerbated through very specific modulations.

A good article showing that a high flux of fructose in the liver can lead to increased de novo lipogenesis through generation of lipogenic substrates, and stimulated expression of lipogenic enzymes, including acetyl-CoA carboxylase (ACC) and fatty acid synthase, these enzymes are pivotal in nature, so they determine whether fatty acids are oxidized, or synthesized. Further to that, there is significant increases in PGC-1 and other uncoupling proteins when you knockout specific sucrose mediated lipogensis pathways. It is very evident that glucose by itself, regardless of how much overconsumption is administered, will be readily oxidized for thermogenesis of the surplus, leading to the classic case of warmer temperature that people associate with high metabolism and mitochondrial health. However, this is not the case when fructose is added in the equation, and to some extent, dietary fat in an excess energy case, for obvious reasons.

I suspect the reason why the combination of glucose and fructose is worse than either individually have to do with different pathways in inducing lipogenesis gene transcription, fructose working directly on hepatocytes and mitochondrial blunting, and glucose through its insulin mediated effect to increase FAS, regardless, even more egregiously, through insulin-resistance independent mechanism. That only touches on fructose's effect on the immediate term, the longer term implications is building up liver and visceral fat reliably, that further exacerbates insulin resistance, TG synthesis, cholesterol syntesis, poor clearance of plasma lipids and sugars, and ultimatley a breakdown of metabolic function.

Miyazaki et. al has done some great work in that regard.

Genetic control of de novo lipogenesis: role in diet-induced obesity

De novo lipogenesis (DNL) is a complex yet highly regulated metabolic pathway, and transcription factors such as liver X receptor (LXR), sterol regulatory element-binding protein-1c (SREBP-1c), and carbohydrate response element binding protein (ChREBP) ...

www.ncbi.nlm.nih.gov

https://www.journal-of-hepatology.eu/article/S0168-8278(21)00161-6/fulltext

https://www.sciencedirect.com/science/article/pii/S0021925820664134

https://www.cell.com/cell-metabolism/fulltext/S1550-4131(07)00335-X?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS155041310700335X%3Fshowall%3Dtrue

 

[Donnea]

The body cannot convert sugar to energy on the spot, or oxidize it for energy, rather the liver prefers to turn it into fatty acids, then estrify it to triglycerides for transport on apolipoprotein B-100 along with cholesterol for storage. Particularly it is fructose, or worse, the combination of fructose and glucose in a short a amount of time that leads to rapid energy conservation rather than energy liberation. The amount of people who have vitamin or mineral deficiencies to disrupt the ATP or oxidation process is almost non-existent, rather it is a biochemical process exacerbated through very specific modulations.

A good article showing that a high flux of fructose in the liver can lead to increased de novo lipogenesis through generation of lipogenic substrates, and stimulated expression of lipogenic enzymes, including acetyl-CoA carboxylase (ACC) and fatty acid synthase, these enzymes are pivotal in nature, so they determine whether fatty acids are oxidized, or synthesized. Further to that, there is significant increases in PGC-1 and other uncoupling proteins when you knockout specific sucrose mediated lipogensis pathways. It is very evident that glucose by itself, regardless of how much overconsumption is administered, will be readily oxidized for thermogenesis of the surplus, leading to the classic case of warmer temperature that people associate with high metabolism and mitochondrial health. However, this is not the case when fructose is added in the equation, and to some extent, dietary fat in an excess energy case, for obvious reasons.

I suspect the reason why the combination of glucose and fructose is worse than either individually have to do with different pathways in inducing lipogenesis gene transcription, fructose working directly on hepatocytes and mitochondrial blunting, and glucose through its insulin mediated effect to increase FAS, regardless, even more egregiously, through insulin-resistance independent mechanism. That only touches on fructose's effect on the immediate term, the longer term implications is building up liver and visceral fat reliably, that further exacerbates insulin resistance, TG synthesis, cholesterol syntesis, poor clearance of plasma lipids and sugars, and ultimatley a breakdown of metabolic function.

Miyazaki et. al has done some great work in that regard.

View attachment 59582View attachment 59583View attachment 59584

Genetic control of de novo lipogenesis: role in diet-induced obesity

De novo lipogenesis (DNL) is a complex yet highly regulated metabolic pathway, and transcription factors such as liver X receptor (LXR), sterol regulatory element-binding protein-1c (SREBP-1c), and carbohydrate response element binding protein (ChREBP) ...

www.ncbi.nlm.nih.gov

https://www.journal-of-hepatology.eu/article/S0168-8278(21)00161-6/fulltext

https://www.sciencedirect.com/science/article/pii/S0021925820664134

https://www.cell.com/cell-metabolis...trieve/pii/S155041310700335X?showall=true[/It

http://It will probably be hard for...y here. Maybe you should troll somewhere else

 

[Alpha]

Read what I wrote again. You practically can't be PUFA free, and of the natural foods one eats they get enough of the so called essential fats that there is no legitimate reason to take more, not because of some inefficiency of converting ALA or because there is some magical ratio of 3 to 6 If there is a need for a partially unsaturated fat oleic acid will be produced by the body to meet it's need. Your appeal to nature can be dissected in a million ways but suffice it to say that if sucrose alone was a driver of disease the fruits with the most sugar would be seen to cause disease, after all the offending compound is copious and a majority of what the fruit is comprised of (besides water). Yet we see over and over again that fruit intake is shown to be protective in almost every scenario. If sugar was so horrible we would not see fruit be of benefit, the micro and so called macro nutrients are not so plentiful that they offset the amount of sugar. Sugar in the diet can be of harm if sugar IS your diet. But most make sugar a part of their diet, it in no way has the harm that PUFA does in small quantities and to say it's a driver of disease is dishonest and poorly thought out.

You seem to be not following the conversation.

First, addressing your claim that there isn't a magical ratio of omega 3 to 6, that is factually incorrect. If you take excess amounts of omega-6, which most people are through hydrogenated vegetable oils, it needs to be supplemented by omega-3 to counter-balance in order to achieve a magical ratio. I have never mentioned that a well-balanced diet consisting of whole foods is not sufficient to meet your essential fatty acid needs.

I have already explained why fruits are not a significant driver of disease, in addition to the micronutrients they provide that are protective from sugar and inflammation, they also offer the ideal 5:1 ratio of sugar to fibers, significantly lowering their glycemic load and index, in addition to the numerous beneficial processes that fiber independently has that is outside the scope of this topic.

You are entitled to your own opinion, but I would concur that all the things I am laying out are both factual supported by scientific literature, and very well thought out.

 

[Alpha]

What are your thoughts on the healthful effects of Dr. Kempner's Rice Diet? While largely glucose in the form of rice, it is very high in fructose from its fruit and additional sucrose. It was employed to cure cardiovascular disease, diabetes, and renal dysfunction.

Walter Kempner, MD - Founder of the Rice Diet - Dr. McDougall

Click to learn about the founder of the rice diet, Dr. Walter Kempner. This incredible diet can be safe and therapeutic for a range of conditions.

www.drmcdougall.com

I would be inclined to say this is not the best diet to treat T2D, however, I would to need to see third party empircal studies done to verify his work before commenting further. Although I have seen some work done in the past that showed glucose alone, or dietary fat alone, even in excess, improved several biomarkers, suggestive that combinations of macronutrients, particularly fat and carbohydrates, or rather the absence of it, tends to favor energy oxidation and shift the biochemical system towards more optimal metabolic function. This could also explain why carnivore diets have reportedly worked so well for many people, anecdotally.

 

[Alpha]

Ah ok I see what we are dealing with now. Figured.

Forum supporting doesn't make one immune to shilling, beware all who read and sway.

I have been on this forum since 2014, who are you?

 

[Alpha]

"Diabetes was named for the excessive urination it causes, and for the sugar in the urine. It was called the sugar disease, and physicians were taught that sugar was the problem. Patients were ordered to avoid sweet foods, and in hospitals they were sometimes locked up to keep them from finding sweets. The practice was derived from ideology, not from any evidence that the treatment helped.

In 1857, M. Piorry in Paris and William Budd in Bristol, England, reasoned that if a patient was losing a pound of sugar every day in 10 liters of urine, and was losing weight very rapidly, and had an intense craving for sugar, it would be reasonable to replace some of the lost sugar, simply because the quick weight loss of diabetes invariably led to death. Keeping patients from eating what they craved seemed both cruel and futile.

After Budd's detailed reports of a woman's progressive recovery over a period of several weeks when he prescribed 8 ounces of sugar every day, along with a normal diet including beef and beef broth, a London physician, Thomas Williams, wrote sarcastically about Budd's metaphysical ideas, and reported his own trial of a diet that he described as similar to Budd's. But after two or three days he decided his patients were getting worse, and stopped the experiment.

Williams' publication was presented as a scientific refutation of Budd's deluded homeopathic ideas, but Budd hadn't explained his experiment as anything more than an attempt to slow the patient's death from wasting which was sure to be the result of losing so much sugar in the urine. The following year Budd described another patient, a young man who had become too weak to work and who was losing weight at an extreme rate. Budd's prescription included 8 ounces of white sugar and 4 ounces of honey every day, and again, instead of increasing the amount of glucose in the urine, the amount decreased quickly as the patient began eating almost as much sugar as was being lost initially, and then as the loss of sugar in the urine decreased, the patient gained weight and recovered his strength.

Drs. Budd and Piorry described patients recovering from an incurable disease, and that has usually been enough to make the medical profession antagonistic. Even when a physician has himself diagnosed diabetes and told a patient that it would be necessary to inject insulin for the rest of his life, if that patient recovers by changing his diet, the physician will typically say that the diagnosis was wrong, because diabetes is incurable." Dr. Ray Peat

High urine glucose levels accompanied by extreme weight loss sounds like Type-1 diabetes to me. That story happened in the mid 19th century, I would love to see a similar observation done today that is well documented in controlled conditions.

Typically, large ingestion of white sugar in the presence of type 1 diabetes would be a death sentence.

 

[ThinPicking]

I have been on this forum since 2014, who are you?

A remarkable contributor, at least.

I try to keep daily sucrose and added sugars below 20g a day, the lower the better. Cakes, donuts, common chocolates and candies, and soft beverages are all out of the question. I do like to have one or two blocks of dark 70% chocolate as dessert. I used to eat fruits quite a lot to substitute my sugar intake, but could not sustain it for a length of time and gave up.

Why. What exactly was your issue?

Parasympathetic regulation can get a little tricky with higher order cognitive function. But it's passing. No pain no gain they say.

 

[Alpha]

Why. What exactly was your issue?

Few reasons why, one, I do not particularly like fruits, but I do like vegetables. The volume I had to eat to feel satiated was seemingly large, given that on multiple occasions eating fruits before bed gave me significantly bad night sweats where I had to change the bed sheets and clothes twice a night in some cases, that I would guess from nocturnal hypoglycemia.

 

[cremes]

Few reasons why, one, I do not particularly like fruits, but I do like vegetables. The volume I had to eat to feel satiated was seemingly large, given that on multiple occasions eating fruits before bed gave me significantly bad night sweats where I had to change the bed sheets and clothes twice a night in some cases, that I would guess from nocturnal hypoglycemia.

Nocturnal HYPOglycemia? Don't you mean HYPERglycemia here? If the fruits were full of sugar (probably) then your liver would likely have sufficient glycogen stores for overnight.

If HYPERglycemic, you could get night sweats because you were burning off excess sugar from the fruit. If HYPOglycemic, the night sweats would be from adrenaline eating through protein to generate sufficient glucose. If *fruit* was causing this issue, the former seems more likely than the latter.

Please clarify because this report doesn't make sense.

 

[CLASH]

This is a very broad question, however I will attempt to explain the biochemical process by which sucrose, to make the distinction more targeted, consumption can lead to inflammation is multifaceted and involves key steps that eventually leads to inflammation, initially transitory, then chronically.

1. Sucrose, a disaccharide composed of glucose and fructose, is quickly broken down in the gut and absorbed into the bloodstream. This rapid absorption can cause spikes in blood sugar levels.

2. The rise in blood glucose triggers the pancreas to release insulin, a hormone that helps cells absorb glucose from the bloodstream for energy. Given the unprocessed nature, and the presence of fructose molecule, it reliably causes the biggest insulin spike of any of the most commonly consumed foods. Overconsumption of sucrose leads to frequent insulin spikes that increases the daily AUC.

3. Unlike glucose, fructose is primarily metabolized in the liver. High intake of fructose (which forms half of sucrose) can overwhelm the liver's processing capacity, leading to several metabolic disturbances:
- Excess fructose can be converted into fats (triglycerides) through DNL. This process can lead to fat accumulation in the liver (non-alcoholic fatty liver disease, NAFLD), which is associated with inflammation and the primary cause of hepatic (and consequently) systemic insuling resistance
- Fructose metabolism can lead to increased production of uric acid, a byproduct that, at high levels, may cause inflammation and oxidative stress.

5. Excess energy and DNL from sucrose leads to the expansion of adipose tissue. Overstretched adipocytes (fat cells) can become hypoxic (low in oxygen) and stressed, releasing pro-inflammatory cytokines and adipokines. This is already well established in CRP for overweight and obese subjects.

6. High blood glucose levels increase oxidative stress, leading to the production of reactive oxygen species (ROS). These ROS can damage cells and tissues, triggering an inflammatory response.

7. Certain components of the immune system, particularly macrophages and other inflammatory cells, can be activated by these metabolic disturbances caused by high sucrose consumption, further exacerbating inflammation.

8. In insulin resistance, there is an increased production of pro-inflammatory cytokines like IL-1β and IL-6. These cytokines are produced in response to prolonged exposure to free fatty acids (FFAs) and glucose, particularly in the β-cells of the pancreas. This production triggers various transcription-mediated molecular pathways, such as TXNIP, MYD88, NF-κB, TLRs, caspases, and inflammasomes, leading to inflammation.

9. In obesity, which often accompanies insulin resistance, the adipose tissue and liver become key sites for inflammation. This is even more true for visceral fat, it's almost 4x as inflammatory as adipose fat, and hepatic fat is 10x as inflammatory as adipose far. In the liver, steatosis, visceral fat, and obesity activate inflammatory signaling pathways, with cytokines and FFAs produced by hepatocytes or abdominal fat tissue potentially activating Kupffer cells (resident hepatic macrophages). This hepatic inflammation is a significant factor in insulin resistance. Fructose (and alcohol sugar) is known to increase hepatic and visceral fat the highest, regardless of calorie consumption.

10. IL-6, a cytokine whose levels are positively correlated with insulin resistance. IL-6 impacts non-oxidative glucose metabolism and lipoprotein lipase activity, influencing plasma triglyceride levels. It also activates the suppressor of cytokine signaling (SOCS) proteins, which can block the activation of the insulin receptor, contributing to insulin resistance as a negative feedback. More specifically, the inflammation response depends on the mechanism. Glucose induces short term postprandial oxidation and associated inflammation, eventually leading to long term insulin resistance, while fructose induces long term insulin resistance and increase in pro-inflammatory cytokine responses through overconsumption from more blunted insulin response, and associated gradual increase in hepatic and visceral fat.

Mechanisms of inflammatory responses and development of insulin resistance: how are they interlinked? - Journal of Biomedical Science

Background Insulin resistance (IR) is one of the major hallmark for pathogenesis and etiology of type 2 diabetes mellitus (T2DM). IR is directly interlinked with various inflammatory responses which play crucial role in the development of IR. Inflammatory responses play a crucial role in the...

jbiomedsci.biomedcentral.com

JCI - Inflammation and insulin resistance

www.jci.org

1.. Starches, which are pure glucose tend to causes higher blood glucose spikes, than sucrose. A look at the glycemic index will show this. Fructose itself doesn't increase blood glucose levels rapidly and doesn't producte a significant insulin response.

2. Larger insulin spikes occur in response to glucose only sources. Its important to be specific about the threshold for an "increase daily AUC" that is actually problematic. Increased carb consumption may increase insulin initially up to a point, but insulin sensitivity also improves leading to less insulin requirements for higher carb intakes.

3.. Only under extreme circumstances in metabolically impaired individuals is the livers capacity impaired. Carbohydrate intake, including fructose contributes very minimally to hepatic DNL. This is well known in the research. It increase trigs by altering peripheral fatty acid metabolism. Multiple things can lead to NAFLD, and multiple different components are required to create the context in which it develops and progresses to NASH. It takes extreme circumstances in healthy individuals to increase Uric acid into problematic ranges. Uric acid is a serum antioxidant.

4.. You missed point #4 and went straight to point #5 from point #3.

5.. Excess energy in general can drive DNL and adipocyte expansion. Sucrose doesn't significantly increase DNL under isocaloric feeding compared to other carbohydrate sources.

6.. High blood glucose levels occur primarily in type 1 and 2 diabetes for different reasons. The ROS mechanism you discuss in this context is most relevant to the type 2 circumstance. The high ROS in type 2 is driven by mitochondrial dysfunction with an overeliance on fatty acid oxidation, leading to an altered cellular uptake and utilization of glucose. Thus the problem isn't glucose ingestion, or fructose ingestion, its disturbed mitochondrial function and excess fatty acid oxidation.

7.. Macrophages are activated by the metabolic dysfunction, which isn't neccesarily directly triggered by glucose or fructose. Theres ancillary sequelae of pure sucrose and pure fructose ingestion that can contribute to metabolic issues but the sugars themselves aren't inherently harmful.

8.. This has little direct relevance to fructose, sucrose, or glucose ingestion. The hyperglycemia from type 2 diabetes is often a function of increased gluconeogenesis from hyperglucagonemia in combination with excess fatty acid oxidation and FFA release.

9.. This happens with free fructose feeding in rat studies, which is not so relevant to normal patterns of fructose consumption in humans.

10.. Exaggerated statements made without supporting mechanisms and evidence mentioned. The jargon about IL-6 was very loosely connected to the lower points at best, but it didn't provide any direct support for the lower statements.

-----

The major concerns with sucrose are its lack of nutrients and possible microbiome disturbance. It shouldn't be a primary carbohydrate source but it doesn't seem to be the smoking gun for disease.

Pure fructose without glucose is worse than sucrose due to its lack of absorption in the intestine and susbequent spurning of endotoxin production. However large amounts of pure fructose without glucose rarely occurs in the diet, even in the US and even with high fructose corn syrup consumption.

The "best" primary sources of carbohydrate from a purely rational nutrition perspective are tubers, and fruits/ juice. These minimize GI irritation, minimize allergens, minimize microbiome disruption, are bioavailable, are nutrient dense (vitamins, minerals, polyphenols, fibers, etc.), minimize hormonal disruption, minimize metabolic disruption and have largely positive outcomes in the research. Dairy is another good source but tolerance varies due to lactose and casein peptides.

Grains and legumes are other possible sources but they can have irritating fibers & allergens, imbalanced micronutrients (high phos)/ lower micronutrients, can negatively impact hormonal function, some can disrupt the microbiome, and in general are much less digestible overall. White rice is a gray area with mixed pros and cons here.

Blaming fructose, sucrose, or carbohydrates as the "cause" of disease, rather than fully understanding the overarching context, often leads to problematic extensions and conclusions.

 

[CLASH]

Correct. Glucose is a toxic and addictive reactive aldehyde.

lol

 

[Razvan]

1.. Starches, which are pure glucose tend to causes higher blood glucose spikes, than sucrose. A look at the glycemic index will show this. Fructose itself doesn't increase blood glucose levels rapidly and doesn't producte a significant insulin response.

2. Larger insulin spikes occur in response to glucose only sources. Its important to be specific about the threshold for an "increase daily AUC" that is actually problematic. Increased carb consumption may increase insulin initially up to a point, but insulin sensitivity also improves leading to less insulin requirements for higher carb intakes.

3.. Only under extreme circumstances in metabolically impaired individuals is the livers capacity impaired. Carbohydrate intake, including fructose contributes very minimally to hepatic DNL. This is well known in the research. It increase trigs by altering peripheral fatty acid metabolism. Multiple things can lead to NAFLD, and multiple different components are required to create the context in which it develops and progresses to NASH. It takes extreme circumstances in healthy individuals to increase Uric acid into problematic ranges. Uric acid is a serum antioxidant.

4.. You missed point #4 and went straight to point #5 from point #3.

5.. Excess energy in general can drive DNL and adipocyte expansion. Sucrose doesn't significantly increase DNL under isocaloric feeding compared to other carbohydrate sources.

6.. High blood glucose levels occur primarily in type 1 and 2 diabetes for different reasons. The ROS mechanism you discuss in this context is most relevant to the type 2 circumstance. The high ROS in type 2 is driven by mitochondrial dysfunction with an overeliance on fatty acid oxidation, leading to an altered cellular uptake and utilization of glucose. Thus the problem isn't glucose ingestion, or fructose ingestion, its disturbed mitochondrial function and excess fatty acid oxidation.

7.. Macrophages are activated by the metabolic dysfunction, which isn't neccesarily directly triggered by glucose or fructose. Theres ancillary sequelae of pure sucrose and pure fructose ingestion that can contribute to metabolic issues but the sugars themselves aren't inherently harmful.

8.. This has little direct relevance to fructose, sucrose, or glucose ingestion. The hyperglycemia from type 2 diabetes is often a function of increased gluconeogenesis from hyperglucagonemia in combination with excess fatty acid oxidation and FFA release.

9.. This happens with free fructose feeding in rat studies, which is not so relevant to normal patterns of fructose consumption in humans.

10.. Exaggerated statements made without supporting mechanisms and evidence mentioned. The jargon about IL-6 was very loosely connected to the lower points at best, but it didn't provide any direct support for the lower statements.

-----

The major concerns with sucrose are its lack of nutrients and possible microbiome disturbance. It shouldn't be a primary carbohydrate source but it doesn't seem to be the smoking gun for disease.

Pure fructose without glucose is worse than sucrose due to its lack of absorption in the intestine and susbequent spurning of endotoxin production. However large amounts of pure fructose without glucose rarely occurs in the diet, even in the US and even with high fructose corn syrup consumption.

The "best" primary sources of carbohydrate from a purely rational nutrition perspective are tubers, and fruits/ juice. These minimize GI irritation, minimize allergens, minimize microbiome disruption, are bioavailable, are nutrient dense (vitamins, minerals, polyphenols, fibers, etc.), minimize hormonal disruption, minimize metabolic disruption and have largely positive outcomes in the research. Dairy is another good source but tolerance varies due to lactose and casein peptides.

Grains and legumes are other possible sources but they can have irritating fibers & allergens, imbalanced micronutrients (high phos)/ lower micronutrients, can negatively impact hormonal function, some can disrupt the microbiome, and in general are much less digestible overall. White rice is a gray area with mixed pros and cons here.

Blaming fructose, sucrose, or carbohydrates as the "cause" of disease, rather than fully understanding the overarching context, often leads to problematic extensions and conclusions.

Clash is back! :)) Where have you been man?

 

[Pete Rey]

View attachment 59581

Normally I'd say attacking someone's credibility instead of their argument is bad form... but this is one hell of an exception. YIKES.

 

[ATP]

sucrose, which is one part glucose, one part fructose, is the main source of metabolic syndrome, which in turn is the umbrella condition that leads to the other more commonly known diseases such as Atherosclerosis Cardiovascular Disease (ASCVD), Dementia, Diabates, Obesity, Stroke, and Renal disease.

If sugar is the "main" cause of disease then it would be considered bad and should be avoided. .

Sufficient energy can only be derived from two macro nutrients, you've ruled sugar to be disease causing.

Dietary protein can not be increased to compensate for the avoidance of sugar as some amino acids are glucogenic and cause blood sugar and insulin spikes.

You have now arrived at a ketogenic diet.

 

[Jamsey]

This is a very broad question, however I will attempt to explain the biochemical process by which sucrose, to make the distinction more targeted, consumption can lead to inflammation is multifaceted and involves key steps that eventually leads to inflammation, initially transitory, then chronically.

1. Sucrose, a disaccharide composed of glucose and fructose, is quickly broken down in the gut and absorbed into the bloodstream. This rapid absorption can cause spikes in blood sugar levels.

2. The rise in blood glucose triggers the pancreas to release insulin, a hormone that helps cells absorb glucose from the bloodstream for energy. Given the unprocessed nature, and the presence of fructose molecule, it reliably causes the biggest insulin spike of any of the most commonly consumed foods. Overconsumption of sucrose leads to frequent insulin spikes that increases the daily AUC.

3. Unlike glucose, fructose is primarily metabolized in the liver. High intake of fructose (which forms half of sucrose) can overwhelm the liver's processing capacity, leading to several metabolic disturbances:
- Excess fructose can be converted into fats (triglycerides) through DNL. This process can lead to fat accumulation in the liver (non-alcoholic fatty liver disease, NAFLD), which is associated with inflammation and the primary cause of hepatic (and consequently) systemic insuling resistance
- Fructose metabolism can lead to increased production of uric acid, a byproduct that, at high levels, may cause inflammation and oxidative stress.

5. Excess energy and DNL from sucrose leads to the expansion of adipose tissue. Overstretched adipocytes (fat cells) can become hypoxic (low in oxygen) and stressed, releasing pro-inflammatory cytokines and adipokines. This is already well established in CRP for overweight and obese subjects.

6. High blood glucose levels increase oxidative stress, leading to the production of reactive oxygen species (ROS). These ROS can damage cells and tissues, triggering an inflammatory response.

7. Certain components of the immune system, particularly macrophages and other inflammatory cells, can be activated by these metabolic disturbances caused by high sucrose consumption, further exacerbating inflammation.

8. In insulin resistance, there is an increased production of pro-inflammatory cytokines like IL-1β and IL-6. These cytokines are produced in response to prolonged exposure to free fatty acids (FFAs) and glucose, particularly in the β-cells of the pancreas. This production triggers various transcription-mediated molecular pathways, such as TXNIP, MYD88, NF-κB, TLRs, caspases, and inflammasomes, leading to inflammation.

9. In obesity, which often accompanies insulin resistance, the adipose tissue and liver become key sites for inflammation. This is even more true for visceral fat, it's almost 4x as inflammatory as adipose fat, and hepatic fat is 10x as inflammatory as adipose far. In the liver, steatosis, visceral fat, and obesity activate inflammatory signaling pathways, with cytokines and FFAs produced by hepatocytes or abdominal fat tissue potentially activating Kupffer cells (resident hepatic macrophages). This hepatic inflammation is a significant factor in insulin resistance. Fructose (and alcohol sugar) is known to increase hepatic and visceral fat the highest, regardless of calorie consumption.

10. IL-6, a cytokine whose levels are positively correlated with insulin resistance. IL-6 impacts non-oxidative glucose metabolism and lipoprotein lipase activity, influencing plasma triglyceride levels. It also activates the suppressor of cytokine signaling (SOCS) proteins, which can block the activation of the insulin receptor, contributing to insulin resistance as a negative feedback. More specifically, the inflammation response depends on the mechanism. Glucose induces short term postprandial oxidation and associated inflammation, eventually leading to long term insulin resistance, while fructose induces long term insulin resistance and increase in pro-inflammatory cytokine responses through overconsumption from more blunted insulin response, and associated gradual increase in hepatic and visceral fat.

Mechanisms of inflammatory responses and development of insulin resistance: how are they interlinked? - Journal of Biomedical Science

Background Insulin resistance (IR) is one of the major hallmark for pathogenesis and etiology of type 2 diabetes mellitus (T2DM). IR is directly interlinked with various inflammatory responses which play crucial role in the development of IR. Inflammatory responses play a crucial role in the...

jbiomedsci.biomedcentral.com

JCI - Inflammation and insulin resistance

www.jci.org

1.. Starches, which are pure glucose tend to causes higher blood glucose spikes, than sucrose. A look at the glycemic index will show this. Fructose itself doesn't increase blood glucose levels rapidly and doesn't producte a significant insulin response.

2. Larger insulin spikes occur in response to glucose only sources. Its important to be specific about the threshold for an "increase daily AUC" that is actually problematic. Increased carb consumption may increase insulin initially up to a point, but insulin sensitivity also improves leading to less insulin requirements for higher carb intakes.

3.. Only under extreme circumstances in metabolically impaired individuals is the livers capacity impaired. Carbohydrate intake, including fructose contributes very minimally to hepatic DNL. This is well known in the research. It increase trigs by altering peripheral fatty acid metabolism. Multiple things can lead to NAFLD, and multiple different components are required to create the context in which it develops and progresses to NASH. It takes extreme circumstances in healthy individuals to increase Uric acid into problematic ranges. Uric acid is a serum antioxidant.

4.. You missed point #4 and went straight to point #5 from point #3.

5.. Excess energy in general can drive DNL and adipocyte expansion. Sucrose doesn't significantly increase DNL under isocaloric feeding compared to other carbohydrate sources.

6.. High blood glucose levels occur primarily in type 1 and 2 diabetes for different reasons. The ROS mechanism you discuss in this context is most relevant to the type 2 circumstance. The high ROS in type 2 is driven by mitochondrial dysfunction with an overeliance on fatty acid oxidation, leading to an altered cellular uptake and utilization of glucose. Thus the problem isn't glucose ingestion, or fructose ingestion, its disturbed mitochondrial function and excess fatty acid oxidation.

7.. Macrophages are activated by the metabolic dysfunction, which isn't neccesarily directly triggered by glucose or fructose. Theres ancillary sequelae of pure sucrose and pure fructose ingestion that can contribute to metabolic issues but the sugars themselves aren't inherently harmful.

8.. This has little direct relevance to fructose, sucrose, or glucose ingestion. The hyperglycemia from type 2 diabetes is often a function of increased gluconeogenesis from hyperglucagonemia in combination with excess fatty acid oxidation and FFA release.

9.. This happens with free fructose feeding in rat studies, which is not so relevant to normal patterns of fructose consumption in humans.

10.. Exaggerated statements made without supporting mechanisms and evidence mentioned. The jargon about IL-6 was very loosely connected to the lower points at best, but it didn't provide any direct support for the lower statements.

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The major concerns with sucrose are its lack of nutrients and possible microbiome disturbance. It shouldn't be a primary carbohydrate source but it doesn't seem to be the smoking gun for disease.

Pure fructose without glucose is worse than sucrose due to its lack of absorption in the intestine and susbequent spurning of endotoxin production. However large amounts of pure fructose without glucose rarely occurs in the diet, even in the US and even with high fructose corn syrup consumption.

The "best" primary sources of carbohydrate from a purely rational nutrition perspective are tubers, and fruits/ juice. These minimize GI irritation, minimize allergens, minimize microbiome disruption, are bioavailable, are nutrient dense (vitamins, minerals, polyphenols, fibers, etc.), minimize hormonal disruption, minimize metabolic disruption and have largely positive outcomes in the research. Dairy is another good source but tolerance varies due to lactose and casein peptides.

Grains and legumes are other possible sources but they can have irritating fibers & allergens, imbalanced micronutrients (high phos)/ lower micronutrients, can negatively impact hormonal function, some can disrupt the microbiome, and in general are much less digestible overall. White rice is a gray area with mixed pros and cons here.

Blaming fructose, sucrose, or carbohydrates as the "cause" of disease, rather than fully understanding the overarching context, often leads to problematic extensions and conclusions.

Beast. I was going to respond but you beat me to it. Well done

 

[Alpha]

Nocturnal HYPOglycemia? Don't you mean HYPERglycemia here? If the fruits were full of sugar (probably) then your liver would likely have sufficient glycogen stores for overnight.

If HYPERglycemic, you could get night sweats because you were burning off excess sugar from the fruit. If HYPOglycemic, the night sweats would be from adrenaline eating through protein to generate sufficient glucose. If *fruit* was causing this issue, the former seems more likely than the latter.

Please clarify because this report doesn't make sense.

I've thought about that as well, I think hypoglycemia was a more probable cause, but I should have had my blood sugar checked then. This has happened almost everytime I eat fruits before bed, and the amount of sweat was astounding, you could wring the bed sheets and clothes from the amount of water I expelled, and it would happen again in the same night.

This usually happens if I eat more than just a few fruits (mainly berries since they are easier to eat), my theory is my insulin sensitivity being not optimal to consume a large amount of fruit, is releasing a large amount of insulin in response to what typically would be in the same amount of processed sugars, and seeing a rubber-band effect where blood sugar suddenly drops a few hours later.

This is just speculation on part, but it has happened consistently enough where I learned to avoid making fruits a main component of my diet.

 

[Alpha]

If sugar is the "main" cause of disease then it would be considered bad and should be avoided. .

Sufficient energy can only be derived from two macro nutrients, you've ruled sugar to be disease causing.

Dietary protein can not be increased to compensate for the avoidance of sugar as some amino acids are glucogenic and cause blood sugar and insulin spikes.

You have now arrived at a ketogenic diet.

Hi ATP. Sugar is a broad term and certainly should not be avoided. That's not to say that sugar is essential, as you have alluded to, the body is excellent at gluconeogenesis and an essential sugar does not exist. What makes carbohydrates different from fatty acids and amino acids, the substrates used for function, is that only one form exists, and that is glucose (glycogen is part of that). Whereas the number of amino acids or fatty acids that the body uses, whether essential or non-essential, are too many to name.

With that said, the main cause of disease is sucrose, one type of sugar, particularly processed sugar. That is undeniable as far as I'mconcerned, if you eliminate processed sugar in the modern world, you reduce annual deaths from the causes I mentioned by significant margin, if not almost eradicating them in otherwise healthy individuals.

Protein is indeed insulingenic, but not nearly to the same extent as chronic sucrose consumption is. In fact, it is impossible to develop insulin resistance eating nothing but protein due to rate-limiting steps for one, and the muted insulin response per gram consumed.

I do not advocate for a ketogenic diet. I personally prefer to have most of my calories from polysaccharides and proteins, preferentially from high quality whole foods.