Acupuncture & Chinese Medicine ● Longevity Nutrition

fructose

 

Chokecherries

In the temperate zones of the Earth, late summer into autumn has been a time of celebration in many cultures. This is the time when all creatures breathe a sigh of relief as the hard work of growth slows. The cooler air transforms summer’s searing rays of sunshine into loving, golden warmth. Pregnant with sugar, fruits of flowering plants hang heavy from the branches and dapple the landscape in a mosaic of reds, blues and purples from anthocyanins and carotenoids. On the ground, combinations of lutein and zeaxanthin color the winter squashes of the Cucurbita family with the same oranges and yellows that are revealed as chlorophyll relinquishes its dominion over the foliage.

Colorful pigments that once acted as a beacon for pollinators in an array of colors and hormones[1] assume a new form that will serve as this year’s bridge of survival for numerous species of birds and mammals, including humans.

Over these precious few weeks, concentrated glucose and fructose flow in like the ocean tide. With them, the stomach’s master hormones of appetite flip flop. Ghrelin’s waxing and leptin’s waning[2] impose an ever-rising voracity of appetite that has driven successful survival of species over hundreds of millions of years. Inside the sweet goodness lurks even more treasures. Fresh omega-six oils from seeds and grains give a fresh boost to dwindling eicosanoids that are crucial for cell-to-cell communication. Vitamin E, selenium[3], vitamin C and phytonutrients stand like a levy to ensure the rising tide of inflammation doesn’t breach its banks.

In Traditional Chinese Medicine Theory, this time of year was considered the fifth season associated with the Earth element.  Warmth, sunshine, water and Earth have been magically transformed by a billion tiny seeds into a form that passes life’s nourishment unto us.   In the Jewish tradition, this season beckons the new year known as Rosh Hashanah.

“Blessed are you, sovereign of the Universe who brings forth bread to the Earth…who has kept us in life, has sustained us and brought us to this season.” Torah

Lurking deep within the cell, all the way down to the nuclear membrane, a sugar-laden surge of insulin nudges a sleeping Goddess from her torpor. 2.1 billion years ago[4],[5] some of the earliest fungi birthed this goddess and time kindly bequeathed her unto humans. In science she is known as SREBP or sterol regulatory elemental binding proteins. She is the one who, as if by magic, signals that transformation of sugar into a form that can be stored for later use as triglycerides[6] and fat[7].  Without her, most animals in the temperate and arctic zones are unlikely to survive even one winter.

Because of SREBP’s, every cell can make its own LDL cholesterol for membrane repair and vitamin D synthesis. However, without a way to supply basic antioxidants to the cell, LDL quickly oxidizes. This transformation from Dr. Jeckel to Mr. Hyde damages everything it touches[8] and is considered to be one of the driving forces of atherosclerosis7. In order to protect her inner world and ensure a constant supply of antioxidants, SREBP must ask for a little help from one of her cousins in the liver, SREBP-1. While most of the cells of the body settle for glucose as an energy source, the liver engages in a more refined taste for fructose. In fact, liver cells are the only ones that can use fructose and its effects are incendiary. Fructose drives rapid production of LDL cholesterol, fats and inflammation in the liver[9],[10]. This preference for fructose acts as a supply chain for the trillions of cells’ insatiable need for antioxidants during times like these. But without SREBP, these antioxidants are useless. She alone is the key master who permits passage of these antioxidants across the cell membrane. Under the dominion of SREBP, the LDL cholesterol receptor rises to the surface of the cell like a fish rising to feed. If it is lucky, LDL cholesterol will land in its mouth. Along for the ride, precious antioxidants like vitamins A, C, and E are granted access to the cell’s inner world[11].

As this season wanes, berries hang dried and scant on the branches. Insulin recedes as the sugar festival comes to a close. The Earth cools. SREBP breathes a deep sigh as her hard work comes to an end. As she falls into her winter nap, she brings many of the creatures of the Earth with her. Only one creature has successfully escaped the dominion of this goddess. Humans innovated to store carbohydrates externally. This consistent supply of sugar drives insulin to ensure that SREBP never sleeps. Her unrelenting state of slavery drives disorders like obesity[12],[13], fatty liver[14], insulin resistance[15] and atherosclerosis[16], [17]. Perhaps this goddess would argue that these are not diseases at all but are phenotypes brought on by depriving her of a proper rest.

[1] Cutler A.J., Krochko J.E. Formation and breakdown of ABA. Trends Plant. Sci. 1999;4:472–478. doi: 10.1016/S1360-1385(99)01497-1

[2] Teff KL, Elliott, SS, Tschop M, Kieffer TJ, Rader D., Heiman M., Townsend RR., Keim NL, D’Alesso D, Havel Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. PJ J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72

[3] Giacomo dugo, Lara La Pera, Donatella Pollicino, marello Saitta. Determination of Selenium Content in Different Types of Seed Oils by Cathodic Stripping Potentiometry (CSP) J. Agric. Food Chem., 2003, 51 (19), pp 5598–5601

[4] Timothy F. Osborne, Peter J. Espenshade Evolutionary Conservation and Adaptation in the Mechanism that Regulates SREBP Action: What a Long Strange tRIP It’s Been. Genes & Dev. 2009. 23: 2578-2591, doi:10.1101/gad.1854309

[5] V Laudet Evolution of the Nuclear Receptor Superfamily: Early Diversification from an Ancestral Orphan Receptor. Journal of Molecular Endocrinology Dec. 1, 1997. 19 2-7-226

[6] Colleen K. Nye  Glyceroneogenesis Is the Dominant Pathway for Triglyceride Glycerol Synthesis in Vivo in the Rat The Journal of Biological Chemistry, 283, 27565-27574.  October 10, 2008

[7] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

[8] Low Density Lipoprotein Can Cause Death of Islet β-Cells by Its Cellular Uptake and Oxidative Modification Miriam Cnop, Jean Claude Hannaert, Annick Y. Grupping, and Daniel G. Pipeleers Endocrinology 2002 143:9 , 3449-3453 http://dx.doi.org/10.1210/en.2002-220273

 

[9] Zhang C, Chen X, Zhu RM, Zhang Y, Tu T, Wang H., Zhao H, Zhao M, Ji YL, Chen YH, Meng XH, Wei W, Xu DX. “Endoplasmic reticulum stress is involved in hepatic SREBP-1c activation and lipid accumulation in fructose-fed mice.” 2012 Aug 3;212(3):229-40. doi: 10.1016/j.toxlet.2012.06.002. Epub 2012 Jun 12.

“ER stress contributes, at least in part, to hepatic SREBP-1c activation and lipid accumulation in fructose-evoked NAFLD.”

[10] Koo HY, Miyashita M, Cho BH, Nakamura MT. Replacing dietary glucose with fructose increases ChREBP activity and SREBP-1 protein in rat liver nucleus. 2009 Dec 11;390(2):285-9. doi: 10.1016/j.bbrc.2009.09.109. Epub 2009 Sep 30.

“Nuclear SREBP-1 was 2.2 times higher in fructose-fed rats than glucose-fed rats.”

[11] Maret G Traber, Herbert J Kayden “Vitamin E is Delivered to Cells via the High Affinity Receptor for Low-Density Lipoprotein” The American Journal of Clinical Nutrition 40: October 1984, pp 747-51.

[12] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

 

[13] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

[14] Moon YA, Liang G, Xie X, Frank-Kamenetsky M, Fitzgerald K, Koteliansky V, Brown MS, Goldstein JL, Horton JD. The Scap/SREBP pathway is essential for developing diabetic fatty liver and carbohydrate-induced hypertriglyceridemia in animals. Cell Metab. 2012 Feb 8;15(2):240-6

[15] Iichiro Shimomura, Robert E. Hammer, James A. Richardson, Shinji Ikemoto, Yuriy Bashmakov, Joseph L. Goldstein,Michael S. Brown

Insulin resistance and diabetes mellitus in transgenic mice expressing nuclear SREBP-1c in adipose tissue: model for congenital generalized lipodystrophy. Genes Dev. 1998 October 15; 12(20): 3182–3194.

[16] Karasawa T, Takahashi A, Saito R, Sekiya M, Igarashi M, Iwasaki H, Miyahara S, Koyasu S, Nakagawa Y, Ishii K, Matsuzaka T, Kobayashi K, Yahagi N, Takekoshi K, Sone H, Yatoh S, Suzuki H, Yamada N, Shimano H. Sterol regulatory element-binding protein-1 determines plasma remnant lipoproteins and accelerates atherosclerosis in low-density lipoprotein receptor-deficient mice. Arterioscler Thromb Vasc Biol. 2011 Aug;31(8):1788-95.

[17] Kurtak, K. Dietary and Nutritional Manipulation of the Nuclear Transcription Factors, PPAR’s and SREBP’s, as a Tool for Reversing the Primary Diseases of Premature Death and Aging. Rejuvenation Research 17-2. April 2014. P 140-44.

 

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In the temperate zones of the Earth, late summer into autumn has been a time of celebration in many cultures. This is the time when all creatures breathe a sigh of relief as the hard work of growth slows. The cooler air transforms summer’s searing rays of sunshine into loving, golden warmth. Pregnant with sugar, fruits of flowering plants hang heavy from the branches and dapple the landscape in a mosaic of reds, blues and purples from anthocyanins and carotenoids. On the ground, combinations of lutein and zeaxanthin color the winter squashes of the Cucurbita family with the same oranges and yellows that are revealed as chlorophyll relinquishes its dominion over the foliage.

Colorful pigments that once acted as a beacon for pollinators in an array of colors and hormones[1] assume a new form that will serve as this year’s bridge of survival for numerous species of birds and mammals, including humans.

Over these precious few weeks, concentrated glucose and fructose flow in like the ocean tide. With them, the stomach’s master hormones of appetite flip flop. Ghrelin’s waxing and leptin’s waning[2] impose an ever-rising voracity of appetite that has driven successful survival of species over hundreds of millions of years. Inside the sweet goodness lurks even more treasures. Fresh omega-six oils from seeds and grains give a fresh boost to dwindling eicosanoids that are crucial for cell-to-cell communication. Vitamin E, selenium[3], vitamin C and phytonutrients stand like a levy to ensure the rising tide of inflammation doesn’t breach its banks.

In Traditional Chinese Medicine Theory, this time of year was considered the fifth season associated with the Earth element.  Warmth, sunshine, water and Earth have been magically transformed by a billion tiny seeds into a form that passes life’s nourishment unto us.   In the Jewish tradition, this season beckons the new year known as Rosh Hashanah.

“Blessed are you, sovereign of the Universe who brings forth bread to the Earth…who has kept us in life, has sustained us and brought us to this season.” Torah

Lurking deep within the cell, all the way down to the nuclear membrane, a sugar-laden surge of insulin nudges a sleeping Goddess from her torpor. 2.1 billion years ago[4],[5] some of the earliest fungi birthed this goddess and time kindly bequeathed her unto humans. In science she is known as SREBP or sterol regulatory elemental binding proteins. She is the one who, as if by magic, signals that transformation of sugar into a form that can be stored for later use as triglycerides[6] and fat[7].  Without her, most animals in the temperate and arctic zones are unlikely to survive even one winter.

Because of SREBP’s, every cell can make its own LDL cholesterol for membrane repair and vitamin D synthesis. However, without a way to supply basic antioxidants to the cell, LDL quickly oxidizes. This transformation from Dr. Jeckel to Mr. Hide damages everything it touches[8] and is considered to be one of the driving forces of atherosclerosis7. In order to protect her inner world and ensure a constant supply of antioxidants, SREBP must ask for a little help from one of her cousins in the liver, SREBP-1. While most of the cells of the body settle for glucose as an energy source, the liver engages in a more refined taste for fructose. In fact, liver cells are the only ones that can use fructose and its effects are incendiary. Fructose drives rapid production of LDL cholesterol, fats and inflammation in the liver[9],[10]. This preference for fructose acts as a supply chain for the trillions of cells’ insatiable need for antioxidants during times like these. But without SREBP, these antioxidants are useless. She alone is the key master who permits passage of these antioxidants across the cell membrane. Under the dominion of SREBP, the LDL cholesterol receptor rises to the surface of the cell like a fish rising to feed. If it is lucky, LDL cholesterol will land in its mouth. Along for the ride, precious antioxidants like vitamins A, C, and E are granted access to the cell’s inner world[11].

As this season wanes, berries hang dried and scant on the branches. Insulin recedes as the sugar festival comes to a close. The Earth cools. SREBP breathes a deep sigh as her hard work comes to an end. As she falls into her winter nap, she brings many of the creatures of the Earth with her. Only one creature has successfully escaped the dominion of this goddess. Humans innovated to store carbohydrates externally. This consistent supply of sugar drives insulin to ensure that SREBP never sleeps. Her unrelenting state of slavery drives disorders like obesity[12],[13], fatty liver[14], insulin resistance[15] and atherosclerosis[16], [17]. Perhaps this goddess would argue that these are not diseases at all but are phenotypes brought on by depriving her of a proper rest.

[1] Cutler A.J., Krochko J.E. Formation and breakdown of ABA. Trends Plant. Sci. 1999;4:472–478. doi: 10.1016/S1360-1385(99)01497-1

[2] Teff KL, Elliott, SS, Tschop M, Kieffer TJ, Rader D., Heiman M., Townsend RR., Keim NL, D’Alesso D, Havel Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. PJ J Clin Endocrinol Metab. 2004 Jun;89(6):2963-72

[3] Giacomo dugo, Lara La Pera, Donatella Pollicino, marello Saitta. Determination of Selenium Content in Different Types of Seed Oils by Cathodic Stripping Potentiometry (CSP) J. Agric. Food Chem., 2003, 51 (19), pp 5598–5601

[4] Timothy F. Osborne, Peter J. Espenshade Evolutionary Conservation and Adaptation in the Mechanism that Regulates SREBP Action: What a Long Strange tRIP It’s Been. Genes & Dev. 2009. 23: 2578-2591, doi:10.1101/gad.1854309

 

[5] V Laudet Evolution of the Nuclear Receptor Superfamily: Early Diversification from an Ancestral Orphan Receptor. Journal of Molecular Endocrinology Dec. 1, 1997. 19 2-7-226

  • [6] Colleen K. Nye  Glyceroneogenesis Is the Dominant Pathway for Triglyceride Glycerol Synthesis in Vivo in the Rat The Journal of Biological Chemistry, 283, 27565-27574.  October 10, 2008

 

[7] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

 

[8] Low Density Lipoprotein Can Cause Death of Islet β-Cells by Its Cellular Uptake and Oxidative Modification Miriam Cnop, Jean Claude Hannaert, Annick Y. Grupping, and Daniel G. Pipeleers Endocrinology 2002 143:9 , 3449-3453 http://dx.doi.org/10.1210/en.2002-220273

 

[9] Zhang C, Chen X, Zhu RM, Zhang Y, Tu T, Wang H., Zhao H, Zhao M, Ji YL, Chen YH, Meng XH, Wei W, Xu DX. “Endoplasmic reticulum stress is involved in hepatic SREBP-1c activation and lipid accumulation in fructose-fed mice.” 2012 Aug 3;212(3):229-40. doi: 10.1016/j.toxlet.2012.06.002. Epub 2012 Jun 12.

“ER stress contributes, at least in part, to hepatic SREBP-1c activation and lipid accumulation in fructose-evoked NAFLD.”

 

[10] Koo HY, Miyashita M, Cho BH, Nakamura MT. Replacing dietary glucose with fructose increases ChREBP activity and SREBP-1 protein in rat liver nucleus. 2009 Dec 11;390(2):285-9. doi: 10.1016/j.bbrc.2009.09.109. Epub 2009 Sep 30.

“Nuclear SREBP-1 was 2.2 times higher in fructose-fed rats than glucose-fed rats.”

 

[11] Maret G Traber, Herbert J Kayden “Vitamin E is Delivered to Cells via the High Affinity Receptor for Low-Density Lipoprotein” The American Journal of Clinical Nutrition 40: October 1984, pp 747-51.

 

[12] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

 

[13] Hitoshi Shimano, SREBPs: physiology and pathophysiology of the SREBP family. The FEBS Journal 2009 276:3 616-621

 

[14] Moon YA, Liang G, Xie X, Frank-Kamenetsky M, Fitzgerald K, Koteliansky V, Brown MS, Goldstein JL, Horton JD. The Scap/SREBP pathway is essential for developing diabetic fatty liver and carbohydrate-induced hypertriglyceridemia in animals. Cell Metab. 2012 Feb 8;15(2):240-6

 

[15] Iichiro Shimomura, Robert E. Hammer, James A. Richardson, Shinji Ikemoto, Yuriy Bashmakov, Joseph L. Goldstein,Michael S. Brown

Insulin resistance and diabetes mellitus in transgenic mice expressing nuclear SREBP-1c in adipose tissue: model for congenital generalized lipodystrophy. Genes Dev. 1998 October 15; 12(20): 3182–3194.

 

[16] Karasawa T, Takahashi A, Saito R, Sekiya M, Igarashi M, Iwasaki H, Miyahara S, Koyasu S, Nakagawa Y, Ishii K, Matsuzaka T, Kobayashi K, Yahagi N, Takekoshi K, Sone H, Yatoh S, Suzuki H, Yamada N, Shimano H. Sterol regulatory element-binding protein-1 determines plasma remnant lipoproteins and accelerates atherosclerosis in low-density lipoprotein receptor-deficient mice. Arterioscler Thromb Vasc Biol. 2011 Aug;31(8):1788-95.

 

[17] Kurtak, K. Dietary and Nutritional Manipulation of the Nuclear Transcription Factors, PPAR’s and SREBP’s, as a Tool for Reversing the Primary Diseases of Premature Death and Aging. Rejuvenation Research 17-2. April 2014. P 140-44.

 

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I will be traveling to Mongolia for a few weeks and don’t expect to have the ability to do any posts. With regards to my series on Sugar’s Contributions to the Evolution, Then Devolution of Humans.   I would like to leave you with a story that demonstrates why it has taken so long for our society to become informed about the adverse health effects of sugar.  Before I start, I would also like to add that when I was traveling through Ecuador a few months ago, every medicine man and shaman that I met said one of the best things you can do to keep your people healthy is to minimize sugar.  They understood that fruit sugar was the same as any other sugar. It’s amazing to me that they didn’t require any scientific evidence for this.  They simply understood.

A few months ago, our nurse practitioner was following a study that was supposed to show that fructose, specifically from agave, had no adverse health consequences.  At the time, she was admittedly hopeful about the outcome because she loves sugar and was convinced that fruit sugar, because it’s natural, couldn’t be that bad.  The study looked at healthy individuals as well as type 2 diabetics.  Each group consumed a controlled amount of agave syrup daily in addition to their regular diets. After just a few weeks the researchers had to abandon the study because the blood markers in both groups (fasting glucose and hemoglobin A1C) continuously rose.  In the diabetics, the numbers reached unsafe levels.  Since the intention of the study was to show that fructose from agave was safe, nothing was published and this valuable information never made it into the scientific literature.

This is a photo of Intipaxi, a traveling healer, whom I met in Ecuador.  He would visit villages and teach the people how to use their local plants medicinally and how to keep themselves healthy. He continually talked about the importance of sunshine and walking barefoot on the Earth.

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Overconsumption of any sugar has deleterious effects on our health.  However, of the primary types of sugars that our cells can utilize; glucose (common in root vegetables and grains), fructose (common in fruit, honey, agave and corn) and galactose (common in legumes and milk) I propose that fructose has the most detrimental effects on human health. Unlike glucose, which is metabolized by most cells as an energy source, fructose is mainly metabolized by liver cells.    As I mentioned in my last post, a study appeared way back in 1988 in the Journal of Diabetes Research and Clinical Practice that showed fructose has a reaction constant 7.5 times higher than glucose as well as a much higher calculated biohazard rating.  Supporting research has increased exponentially since then.

In small amounts AND in the presence of adequate antioxidants, the liver has no problem metabolizing fructose.  In fact, it converts it into glycogen which is the primary fuel for anaerobic muscles (the ones that get really big when you lift weights).  Any fructose left after the muscles have had their fill of glycogen is converted into triglycerides.  These “feed” fat cells for later use.  Depending on which study you read, this occurs if more than 5-7 grams of fructose is consumed in one sitting. In addition to being converted into triglycerides, the excess fructose initiates a damaging, inflammatory response in the liver along with producing elevated levels of free radicals known as reactive oxygen species (ROS).

Here is a brief summary of the amounts of sugar contained in one cup of various fruits and beverages:  Please note that I couldn’t find a breakdown of the glucose to fructose ratio.  Source: http://nutritiondata.self.com/

  • Coke                      (26g sugar) – almost all fructose
  • Bananas               (28g sugar)
  • Apples                 (13g sugar)
  • Apple juice         (24g sugar) – 15 grams of fructose
  • Grapes                 (23g sugar)
  • Apricots               (14g sugar)
  • Cherries               (15g sugar)
  • Grapefruit            (17g sugar)
  • Cantaloupe         (14g sugar)
  • Pears                     (16g sugar)
  • Plums                    (16g sugar)
  • Blueberries         (15g sugar)
  • Blackberries       (7g sugar)
  • Raspberries        (5g sugar)
  • Peaches               (13g sugar)

At first, the inflammation and free radical activity initiated in the liver from fructose results in fat accumulation inside the cells and mildly reduced function. If it continues along this path for any amount of time, a condition called non-alcoholic fatty liver disease, NAFLD, develops.  Scores of studies demonstrate that along with obesity, NAFLD incidence has been steadily rising in Westernized, developed countries and in counties that are becoming developed.   A study showed a 10-year doubling of NAFLD in one Chinese Population and demonstrated that a similar trend was seen in both Korea and Japan.

Note:  I thought it would be interesting to compare fructose consumption and NAFLD incidence in various countries.  I spent several hours and had a research assistant spend several more hours trying to find information on fructose sales or consumption in various countries. The information is very difficult and seemingly expensive to obtain.  If anyone has access to this type of information, please contact me or enjoy the dissertation subject. 

I would like to point out that many of these studies are performed by checking serum levels of the liver enzymes ALT and AST.  The pathological changes occur way before these enzymes levels begin to rise.  According to Dr. Michael Cave, a professor of hepatology, gastroenterology and nutrition at the Univerisity of Louisville, ALT and AST parameters should be much lower because these enzymes only begin to increase long after the inflammation and fat accumulation starts.  To be objective, Dr Cave also presents a strong case for an increase in fatty liver disease as a result of chronic exposures to several persistent organic pollutants  and xenobiotics.  Several studies show that exposing liver cells to fructose, then adding a xenobiotic, results in accelerated inflammation and disease.  It is possible that the rise of fatty liver disease has been a combination of increased fructose intake and exposure to these various environmental pollutants that are now ubiquitous in our environment.

Depending on which study you read, NAFLD is seen in 10-24% of America’s general population and 57-74% of obese individuals.  According to the Mayo Clinic’s website, they describe fatty liver disease as “common and for most people causes no signs, symptoms or complications”.  However, long before any physical symptoms present, the liver’s various functions diminish.  If this continues permanent liver damage occurs along with the cumulative toxicity effects of secondary dysfunction.  In addition, any persistent organic compounds that aren’t removed from the blood by the liver accumulate in fat tissue.

Here is a brief summary of the main functions of the liver:

  • Eliminating endogenous toxins like testosterone and estrogen
  • Eliminating exogenous toxins like gasoline vapors, prescription medications, pesticides, artificial fragrances, hormones from birth control usage that are now in the water supply and BPA from the PVC pipes that carry our water.
  • Generating antioxidants like glutathione which not only carry out Phase 2 detoxification in the liver but neutralize pollutants in the lungs and assist with the recycling of neurotransmitters in the nervous system
  • Metabolizing fat along with various types of cholesterol
  • Generating proteins and enzymes for physiological functions all over the body

It makes me cringe to think what is happening to the livers of those poor souls who become motivated to lose a few extra pounds.  They go running five miles per day, lift weights then drink a bunch of carrot juice or eat a banana because they’ve been misinformed into thinking it’s healthy.  Not only are they putting an extra burden on their liver to metabolize the fat that is being burned, they also have to detoxify the various persistent organic compounds that are released from that fat.  For the final assault they add massive doses of fructose.  It would be really interesting to check the liver enzyme levels on NBC’s “The Biggest Loser” contestants before and during the competition.  If I were them, I would do things to support the poor liver like eating more protein and vegetables, getting rid of the fruit and adding supplements like phosphatidylcholine, folic acid, B6, B12, alpha lipoic acid and N-acetyl cystiene.

Clearly, we evolved with the ability to eat fruit.  For the next post in this series, I will discuss this seeming idiosyncrasy along with how the rise of fructose consumption is causing us to devolve.

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Before I begin this first section of my series on sugar, I would like to note that I usually provide references for everything I write.  The information below is based on my daytime profession and years of assembling research.  It would take me too long to find all the references.  However, most of the facts on physiology can be obtained from any basic cell biology book. There are also several books available that are well-researched with solid references.  Here are a couple:  Transcend by Terry Grossman M.D. and Ray Kurzweil and The Zone by Barry Sears.

In our medical office where I’ve practiced longevity nutrition for over ten years, the term “The White Satan” (conceived by Terry Grossman, M.D.) is used synonymously with sugar.  Efforts to educate our “ever-expanding” population about the powerfully, deleterious health effects of sugar consumption have been like turning the Titanic.  The information has been clear and out there for at least 12-15 years but the emergence of sugar-induced obesity and its accompanying diseases; diabetes, high blood pressure, fatty liver disease, heart disease etc. has continued to increase in numbers.  The average age of people affected by these diseases has been falling steadily and it is no longer uncommon for teenagers to be diagnosed with type 2 diabetes.  Several factors have contributed to this trend.

  • Sugar’s highly addictive nature
  • The emergence of an entire monoculture-based industry providing the public with cheap, foods and  sweetened drinks packed full of high-fructose corn syrup
  • The false belief that fruit and fruit juice is healthy
  • Emphasis on starches and fruit on the Food Pyramid
  • The non-evidence-based, low-fat revolution which led people to believe that anything that didn’t contain fat, especially saturated fat, was good for them
  • Slow, weak and uninformed efforts to educate the public

Any time the level of sugar in the blood surpasses what the cells are capable of managing several problems occur. 

  • Inflammation – the hormone insulin is released by the pancreas into the blood to enable our cells to turn sugar into energy.  We obviously need insulin to survive.  However, excessive levels tend to magnify any inflammatory responses that are happening in the body.  In addition, sugar itself, especially fructose, causes direct inflammation in the liver.  Simply eliminating sugar from one’s diet will almost always result in improvement of inflammatory conditions like asthma, acne, and even back pain.
  • Elevated triglycerides – Insulin signals the liver converts excess sugar floating around in the blood into triglycerides.  Unless you possess a rare, genetic disorder, elevated blood sugar is the ONLY physiologic mechanism for producing triglycerides.
  • “Feeding” of fat cells – Triglycerides floating around in the blood are the direct contributor to “feeding” fat cells.  The higher the blood sugar goes, the higher the triglycerides and the faster weight gain occurs.
  • Immune system dysfunction – As pointed out in Transcend, excess sugar interferes with the ability of white blood cells to utilize vitamin C to carry out a proper immune response
  • Intestinal Dysbiosis – Excess sugar changes the body’s terrain, feeding and promoting overgrowth of yeast along with unbeneficial and some pathogenic bacteria.  The inflammatory response that results from the immune system fighting these critters has an effect on the entire body.  It can manifest as various diseases as the inflammatory chemicals make their way through the lymphatic system. 
  • Advanced Glycated Endproducts (AGE’s) -Glycation is a caramelizing, chemical reaction that occurs when sugars come into contact with proteins.  This reaction can be demonstrated easily in a Petri dish or seen when we bake a chicken and the skin becomes brown and crispy.  The same thing happens to our tissues upon exposure to sugar.  Glycation causes gumming up of enzymes and tissues which render them functionless. 

**Good story:  When I was in college, a gross human anatomy class was lucky enough to have an elderly lady as their study subject.  One of the first things the professor pointed out was the amount of glycation in her tissues.  If you sliced through a piece of her lung or liver, it was never difficult to find these areas of brown, crispy, glycated tissue.  Many age spots are the result of glycation.

It is important to know that these “excess” levels of sugar occur when a healthy human consumes more than 5-7 grams of sugar within a given meal.  Diabetics can tolerate 0-5 grams depending on the severity of their insulin resistance.   The glycemic index  is a useful gauge of how quickly a food raises blood glucose levels.  For example a medium, white potato releases glucose into the bloodstream very quickly and is the equivalent of eating 26 grams of sugar.  The glycemic load  is a measurement of the net glucose-release into the system.  For example, if you eat just a bite or two of that high-glycemic potato, the blood glucose goes up just a little.  I’ve noted that most of my readers are incredibly sophisticated in the thinking and I’m sure most have known about the glycemic index and glycemic load for more than a decade.  However, if you somehow missed out, I strongly encourage you to familiarize yourself with it and take it seriously. One teaspoon of sugar is approximately 5 grams. One teaspoon of honey is 6.5 grams of sugar.  A banana contains 28 grams of sugar. 

Here is a link to the most dangerous foods in America http://www.rense.com/general91/20_Worst_Drinks_in_America_2010.pdf

A severe misconception that has resulted from the spotlight shining on the glycemic index is that fruit and fruit sugar is healthy and safe because it has a low glycemic index.  Fruit contains a completely different sugar, fructose, which cannot be measured with a glucose meter.   A study appeared way back in 1988 in the Journal of Diabetes Research and Clinical Practice that showed fructose has a reaction constant 7.5 times higher than glucose as well as a much higher calculated biohazard rating.  Since then, there is a 1000 fold increase in the research that confirms these findings about the dangers of fructose. This information is just reaching the fringes of the mainstream now.  How sad.  In the next post, we will explore this further and then go on to discuss how the emergence of fructose in the Western diet has led to a rapid devolution.  Later I will present a hypothesis that fructose availability was a primary contributing factor to lifespan and longevity throughout the evolution of humans.

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