Thursday, February 25, 2021

High Fructose Sweetener is Toxic Swill, an alleged “Food Product” & Implicated in Sickness Fuel by the Covid Virus

Armenia & possible coup in the works? As the remake agenda progresses under the progressive Biden regime. 

From earlier today

High Fructose Sweetener- Disgusting and it's everywhere. It's been implicated time and time again with inflammation in our bodies. This inflammation causes diabetes. Cancer. And has been fueling the sickness induced by Covid. 

Revisit the PFYT report from December 2020:  Vitamin D and COVID 19: The Evidence for Prevention and Treatment of Coronavirus (SARS CoV 2)

We do not consume high fructose sweetener regularly. (Though it's hard to avoid and is include in many more products then it should be- so watch out for it)  This product is toxic beyond belief. And inflammatory. 

HFCS and sugar have been shown to drive inflammation, which is associated with an increased risk of obesity, diabetes, heart disease, and cancer. In addition to inflammation, excess fructose may increase harmful substances called advanced glycation end products (AGEs), which may harm your cells ( 21 , 22 , 23 ).Sep 27, 2019
Study after study are taking their place in a growing lineup of scientific research demonstrating that consuming high-fructose corn syrup is the fastest way to trash your health.

 Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation


Fructose intake has increased substantially throughout the developed world and is associated with obesity, type 2 diabetes and non-alcoholic fatty liver disease. Currently, our understanding of the metabolic and mechanistic implications for immune cells, such as monocytes and macrophages, exposed to elevated levels of dietary fructose is limited.

See previous post. Entirely

Here, we show that fructose reprograms cellular metabolic pathways to favour glutaminolysis and oxidative metabolism, which are required to support increased inflammatory cytokine production in both LPS-treated human monocytes and mouse macrophages. A fructose-dependent increase in mTORC1 activity drives translation of pro-inflammatory cytokines in response to LPS. LPS-stimulated monocytes treated with fructose rely heavily on oxidative metabolism and have reduced flexibility in response to both glycolytic and mitochondrial inhibition, suggesting glycolysis and oxidative metabolism are inextricably coupled in these cells. The physiological implications of fructose exposure are demonstrated in a model of LPS-induced systemic inflammation, with mice exposed to fructose having increased levels of circulating IL-1β after LPS challenge. Taken together, our work underpins a pro-inflammatory role for dietary fructose in LPS-stimulated mononuclear phagocytes which occurs at the expense of metabolic flexibility.


Typically, activation of the human innate immune system requires the rewiring of cellular metabolic pathways largely to favour glucose metabolism1,2,3,4,5. However, in the various nutrient environments they inhabit, monocytes will be exposed to a range of different carbon sources, the availability of which will likely dictate their metabolism and phenotype. One such carbon source is fructose, the second most abundant dietary sugar found in humans. Fructose is metabolised by glycolysis either by ketohexokinase producing fructose-1-phosphate, a substrate for aldolase B6 (in the liver, kidneys and intestines for example) or converted to the glycolytic intermediate fructose-6-phosphate by hexokinase (HK), albeit at a lower rate than glucose7,8.

 Fructose intake has increased substantially throughout the Western world, largely attributed to elevated sucrose and high fructose corn syrup consumption9 and is thought to exacerbate various non-communicable conditions such as obesity, type 2 diabetes and non-alcoholic fatty liver disease9. Chronic fructose consumption in these conditions has recently been shown to drive hepatic fructolysis, where the expression of lipogenic genes is enhanced10,11,12.

Typically, physiological levels of fructose in the circulation range from 0.04 to 0.2 mM13; however, there are several pathophysiological scenarios in which levels of fructose are elevated. For example, peripheral blood levels can exceed 1 mM in patients with haematological malignancies such as acute myeloid leukaemia and acute lymphoblastic leukaemia14. In addition, fructose concentrations in the bone marrow microenvironment of haematological cancer patients can reach up to 5 mM14. Alterations in the glucose to fructose ratio, particularly when glucose is scarce, enables acute myeloid leukaemia blasts to significantly enhance fructose uptake14. Localised mouse tissue microenvironments, such as the liver, kidneys and jejunum, also have elevated levels of fructose metabolism15. Therefore, there are various pathophysiological scenarios and tissue microenvironments where monocytes will be exposed to either equimolar concentrations of fructose and glucose or concentrations of fructose exceeding that of glucose
The impact of elevated fructose exposure on the immune system has not been investigated extensively. Chronic fructose exposure in rats results in a more inflammatory phenotype of bone marrow mononuclear cells16. While there is some evidence that lipopolysaccharide (LPS)-stimulated human dendritic cells are able to produce enhanced levels of pro-inflammatory cytokines when cultured in fructose as opposed to glucose, the underlying metabolic rewiring that enables this pro-inflammatory phenotype has not been investigated17.

Here we characterise how human monocytes and mouse macrophages respond metabolically and functionally to fructose exposure. We show that activated mononuclear phagocytes demonstrate plasticity in engaging metabolism of this alternative carbon source, yet it leaves the cells metabolically inflexible and vulnerable to further metabolic challenge. Fructose exposure reprogrammes cellular pathways to favour glutaminolysis and oxidative metabolism, which support an inflammatory phenotype in both human and mouse mononuclear phagocytes. Finally, we demonstrate that a short-term high fructose diet promotes inflammation in vivo, suggesting that our findings have pathophysiological significance.
Fructose exposure promotes an oxidative phenotype

We sought to investigate the metabolic response to fructose exposure in activated human monocytes in comparison to other monosaccharides (glucose and galactose) or complete sugar withdrawal. Galactose has been used previously to promote oxidative phosphorylation (OXPHOS) in T cells by reducing glycolysis18. Using the Seahorse Bioanalyzer, we initially injected the monosaccharide (glucose, fructose or galactose) or media control containing no sugar. After 1 h, monocytes were stimulated with LPS and the corresponding extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) were used to measure glycolysis and OXPHOS, respectively, for the duration.

Monocytes incubated with glucose demonstrated a robust increase in basal and LPS-induced ECAR (Fig. 1A). By contrast, monocytes treated with fructose or galactose had low baseline levels of glycolysis, only slightly greater than no sugar controls (Fig. 1A). In addition, monocytes treated with fructose, galactose or no sugar had only a modest increase in ECAR post-LPS exposure (Fig. 1A). Upon activation, glucose-treated cells reduced their OCR, consistent with the reported metabolic switch from OXPHOS to glycolysis upon activation3. Monocytes treated with fructose, galactose or no sugar had an initial burst of increased oxygen consumption and maintained higher OCR for the duration of the assay (Fig. 1B). This demonstrates metabolic flexibility of human monocytes, in this case towards OXPHOS when the cells are unable to engage in glycolysis.
I'll have more information on the affects of  the toxic swill Fructose Sweetener on your immune system at a later date.


  1. Wow! - you range very widely! I would be interested to learn your option regarding the issue of (refined) "sugar" vs HFCS.

    At one end we have the claim that "sugar is sugar" - drinking a can of coke has the same metabolic impact as eating a handful of raisins (29 grams of "natural sugar" per serving).

    Numerous other more nuanced positions are out there as well. That "fructose" is the principle culprit and refined sugar is somehow less injurious as it is a mix of glucose and fructose - and the two are digested at the molecular level very differently. Others claim that eating an apple vs drinking a glass of unsweetened apple juice is entirely different metabolically - the fructose apple juice hits the pancreas directly whereas the fiber and cellulose in the apple bind with the sugars and carry them into the lower large intestine teaming with bacteria which do the digestion thus relieving the pancreas of much metabolic stress.

    I have read, by the way,that upper portions of the large intestine are close to sterile - that is, no bacteria. The lower portions is where the bacteria thrive - it IS in large part - the immune system. What an amazing organ!

    I will check back

    1. Hi RegretLeft:

      Before Covid, though it's still related, health and food were core topics here. As well geopolitical remake of the MENA/Asian region as a a block between Russia and China..

      I don't buy into the sugar is sugar talk.
      And think if you're going to consume sugar you should stick to as close to eating the sugar as it naturally occurs. So an apple is good.
      And orange is good.
      Likely better then drinking the juice.
      Honey and Maple Syrup are preferable to 'table sugar'

      And absolutely stay away from highly processed foods.
      Pop for example (soda) That's toxic and should either never be consumed or should only be consumed in minuscule quantities.


  2. Hi - obviously the sugar-is-sugar position is convenient and reiterated by HFCS producers - but I know of one well respected alt-med practitioner who endorses it - and magnifies it: "sugar-is-sugar-is-sugar"

    One nutritionist - Gary Taubs (? sp) has generalized your position - ALL refined, concentrated foods should be avoided - squeezing an orange is a form of refinement - leaving the cellulose behind - gravy is big no no - slice of roast beef is bad enough but deadly drenched in gravy.

    I have almost conquered my moderate coca-cola habit - but am still trying to figure out whether Pepsi with "real sugar" is any less deleterious than Pepsi with HFCS.

    Ah - "pop" - that's right you are Canadian - I went to grad school in Edmonton and hiked 1,800 miles in eastern Canada the first 15 years of this century. Tobermory is my little heaven ... to which I will never return - covid denier (and test resistor) that I am.

    1. HiRegretLeft:

      It seems to me it's best to eat your food as close to real as possible.
      sugar is sugar makes about as much sense as fats being fats- Where there are variations in fats.
      saturated and it's variants
      poly unsaturated
      mono unsaturated
      It's just not that simple.

      Yup, Canadian!

      Tobermory?- You hiked the Bruce Trail then?

      I've been on parts of it here and their along the escarpment, but, never done the entire stretch of it.

      It's lovely around Niagara,(Niagara region) which is where I reside. Most often we walk in Short Hills, or St Johns
      or any of the other parks that dot the escarpment area.
      There's Rockway too. (just remembered that)
      Then there's the beaches..

      Are you still in Canada?

      btw: hopefully you can resolve the pop issue?
      the odd time I do consume it, it's usually ginger ale

    2. So you have never hiked the trail on the Bruce Peninsula?!

      Do get up there! - Many people claim that 2 or 3 Km in Bruce National Park have the finest scenery on the entire trail - you walk along high cliffs looking out on Georgian Bay - I think the stretch from Wiarton to Tobermory is about 100km - I have hiked all of it except some stretches on roads - multiple times in the Park. There are some fine waterfalls in the Owen Sound area, as well.

      I am a US citizen, resident in the US. My point was that entry to Canada (as I understand it) now requires proof of vaccination or a "negative test" - as well as quarantine?

      I do not think that will change; I will not, of course, submit to vaccination; I will not allow my person to be penetrated by the state; Ergo: I will never return to Canada.

      How about the North Shore of Lake Superior? - The drive on Rt 17 from Sault Ste Marie to Batchawana Bay is the most gorgeous stretch of roadway in Eastern Canada - the drive east from Quebec City to Forillon National Park is a close rival - the Gulf of Saint Lawrence on your left and the seaside mountains towering over you on the right!

      I know eastern Canada from Superior to Fogo Island NFLD.... ah so sad! I have some fond memories of Spruce Up the Bruce day in May - volunteer work parties - I gave back some.

      I am learning much from your work - nice little virtual community.

    3. So you have not hiked the trail on the Bruce Pn? - Do so! - Lots of people claim the finest scenery on the entire trail is to be found along 2,3 Km in Bruce National Park - you walk along high cliffs overlooking Georgian Bay, natural stone arch... the shoreline waters are a gorgeous shade of turquoise (in the sunshine) - oh!
      No, I am a US citizen residing in the US. My point was that entry to Canada now requires proof of vaccination or a "negative test" and/or? quarantine ... Does anyone think that will change anytime soon? (Klaus has said "we can never go back...") ... (I of course will not be vaccinated nor will I allow my person to be penetrated by the state... so I am stuck here - never to return to Canada) ... I "know" Eastern Canada from Superior to Fogo Island NFLD .... hiking there was the joy of my life for 15 years ... ah! - but other people have suffered so much more... I will be strong and resilient.

    4. RegretLeft:

      I've let both comments through and will get back to you
      Thank you for leaving them both :)