Category Archives: Glucose Control


Syzygium cumini: A Tree from the Indian Subcontinent with Multiple Health Benefits

Syzygium cumini, also known as jambul, jambolan, jamblang, or jamun, is an evergreen tropical tree in the flowering plant family Myrtaceae.  Syzygium cumini is native to the Indian Subcontinent and adjoining regions of Southeast Asia. The species ranges across India, Bangladesh, Pakistan, Nepal, Sri Lanka, Malaysia, the Philippines, and Indonesia.  


Syzygium cumini Tree

The name of the fruit is sometimes mistranslated as blackberry, which is a different fruit in an unrelated family.  In southern Asia, the tree is venerated by Buddhists, and it is commonly planted near Hindu temples because it is considered sacred to Lord Krishna.

The compounds in the tree, including the leaves, fruit, seeds and bark, include:  1

  • Anthocyanins
  • Glucoside
  • Ellagic acid
  • Isoquercetin
  • Kaemferol
  • Myrecetin

The fruit contains:

  • Raffinose
  • Glucose
  • Fructose
  • Citric acid
  • Mallic acid
  • Gallic acid
  • Anthocyanins
  • Delphinidin-3-gentiobioside
  • Malvidin-3-laminaribioside
  • Petunidin-3-gentiobioside
  • Cyanidin diglycoside
  • Petunidin
  • Malvidin

The seeds of the fruit contain:

  • Jambosine
  • Glycoside jambolin

The plant has been considered an anti-diabetic medicinal remedy throughout the Indian and Asian populations.  During the last four decades, numerous folk medicinal reports on the anti-diabetic effects of this plant have been cited in the literature. 

The Table below lists the various folk medicine uses of Syzygium cumini:

Folk medicinal uses of S. cumini (L.) Skeels.
Ethnic group used and their origin Plant part used, mode of preparation, administration and ailments treated References
Local people in southern Brazil Either infusions or decoctions of leaves of jambolan in water at an average concentration of 2.5 g/L and drank it in place of water at a mean daily intake of about 1 liter are used in the treatment of diabetes. [74]
Lakher and Pawi in North east India Infusion of fruit or mixture of powdered bark and fruit is given orally to treat diabetes. [75]
  Juice obtained from the seeds is applied externally on sores and ulcers.  
  Powdered seeds are mixed with sugar are given orally 2–3 times daily in the treatment of dysentery.  
  The juice of leaves is given orally as antidote in opium poisoning and in centipede bite.  
  The juice of ripe fruits is stored for 3 days and then is given orally for gastric problems.  
  The juice obtained from the bark is given orally for the treatment of women with a history of repeated abortion.  
Local informants in Maharastra, India Fruit and stem bark are used in the treatment of diabetes, dysentery, increases appetite and to relieve from headache [76]
Nepalese, Lepchas and Bhutias in northeast India Decoction of stem bark is taken orally three times a day for 2–3 weeks to treat diabetes [77]
Native amerindians and Quilombolas in North eastern Brazil Leaves are used in the treatment of diabetes and renal problems. [78]
Kani tribals in Southern India Two teaspoon of juice extracted from the leaf is mixed with honey or cow’s milk and taken orally taken twice a day after food for 3 months to treat diabetes. Fresh fruits are also taken orally to get relief from stomachache and to treat diabetes. [79]
  Young leaf is ground into a paste with goat’s milk and taken orally to treat indigestion.  
Malayalis in South India Paste of seeds is prepared with the combination of leaves of Momordica charantia and flowers of Cassia auriculata and taken orally once a day for 3 months to treat diabetes. [80]
Traditional medical healers in Madagascar Seeds are taken orally for generations as the centerpiece of an effective therapy for counteracting the slow debilitating impacts of diabetes. [35]
Local population in Andhra Pradesh, India Shade dried seeds are made into powder and taken orally thrice a day in the treatment of diabetes. [81]
Siddis in Karnataka, India The juice obtained from the leaves is mixed with milk and taken orally early in the morning, to treat diabetes. [82]
  The juice obtained from the stem bark is mixed with butter milk and taken orally every day before going to bed to treat constipation. The same recipe, when taken early in the morning on an empty stomach, is claimed to stop blood discharge in the faeces.  
Rural population in Brazil Leaves of jambolan are taken orally in the treatment of diabetes. [64]
Traditional healers in Brazil

Tea prepared from the infusion or decoction of leaves is taken orally to treat diabetes.


Tribal people in Maharastra The tender leaves are taken orally to treat jaundice. It was claimed that the eyes, nails and urine turned yellow. The treatment was followed for 2–3 days by adults and children as well. [84]

(Source:  Asian Pac J Trop Biomed. 2012 Mar; 2(3): 240–246.  doi:  10.1016/S2221-1691(12)60050-1)

The fruits, seeds and stem bark of Syzygium cumini possess promising activity against diabetes mellitus which has been confirmed by several experimental and clinical studies and considered its primary health benefit.

There are additional important health benefits of Syzygium cumini that have been studied and published.  They are listed in the Table below:

Health Benefits of Syzygium cumini (Jamun)

A dose which consisted of 20.0 g tannins/kg rat weight showed significantly lower stomach free radical concentrations. These findings suggest that tannins extracted from S. cumini have gastroprotective and anti-ulcerogenic effects.1
These observations established the anti-inflammatory effect of S. cuminii seed extract in exudative, proliferative and chronic stages of inflammation along with an anti-pyretic action. Antiinflammatory and related actions of Syzigium cumini seed extract 2
The study concluded that S. cumini exhibits inhibitory role on inflammatory response to histamine, 5-HT and PGE2.3
The present study demonstrated that S. cumini bark extract has a potent anti-inflammatory action against different phases of inflammation without any side effect on gastric mucosa.4
Anti-bacterial and Anti-fungal
The water and methanolic extracts of Syzygium jambolanum seeds were examined for antibacterial and antifungal activity in vitro using the disc diffusion method, minimum inhibitory concentration, minimum bactericidal concentration and minimum fungicidal concentration. 5
The leaf essential oils of Syzygium cumini and Syzygium travancoricum were tested for their antibacterial property. The activity of S. cumini essential oil was found to be good, while that of S. travancoricum was moderate.6
The radioprotective activity of the hydroalcoholic extract of jamun seeds (SCE) was studied in mice exposed to different doses of gamma radiation. The mice were injected with 0, 5, 10, 20, 40, 60, 80, 100, 120, 140 or 160 mg/kg body weight of SCE, before exposure to 10 Gy of gamma radiation, to select the optimum dose of radiation protection.
The mice treated with 80 mg/kg body weight SCE intraperitoneally before exposure to 6, 7, 8, 9, 10 and 11 Gy of gamma radiation showed reduction in the symptoms of radiation sickness and mortality at all exposure doses and caused a significant increase in the animal survival when compared with the concurrent double distilled water (DDW) + irradiation group. The SCE treatment protected mice against the gastrointestinal as well as bone marrow deaths and the DRF was found to be 1.24.
Syzygium cumini Linn. and Eugenia cumini (SCE) provided protection against the radiation-induced bone marrow death in mice treated with 10-60 mg/kg b.wt. of SCE. However, the best protection was obtained for 30 mg/kg b.wt. SCE, where the number of, survivors after 30 days post-irradiation was highest (41.66%) when compared with the other doses of SCE.8
These data showed that in addition to 5 anthocyanidins, jamun contains appreciable amounts of ellagic acid/ellagitannins, with high antioxidant and antiproliferative activities.9
The leaves, bark and fruits of Terminalia arjuna, Terminalia bellerica, Terminalia chebula and Terminalia muelleri, the leaves and fruits of Phyllanthus emblica, and the seeds of Syzygium cumini were found to have high total phenolic contents (72.0-167.2 mg/g) and high antioxidant activity (69.6-90.6%).10
From the results, using different free radical-scavenging systems, it can be said that the fruit skin of S. cumini have significant antioxidant activity. In each case, lower antioxidant values, in comparison to tea, might be due to drying condition; through which some of antioxidants are presumably degraded. The antioxidant property of the fruit skin may come in part from antioxidant vitamins, phenolics or tannins and/or anthocyanins. Consumption of S. cumini fruit may supply substantial antioxidants which may provide health promoting and disease preventing effects.11
The present study reveals the efficacy of Eugenia jambolana seed kernel in the amelioration of diabetes, which may be attributed to its hypoglycemic property along with its antioxidant potential. The antioxidant effect of Eugenia jambolana seed kernel was also compared with glibenclamide, a standard hypoglycemic drug.12
Diabetes/Blood glucose
The present study reveals the efficacy of Eugenia jambolana seed kernel in the amelioration of diabetes, which may be attributed to its hypoglycemic property along with its antioxidant potential. The antioxidant effect of Eugenia jambolana seed kernel was also compared with glibenclamide, a standard hypoglycemic drug.13
In view of the knowledge summarized here, a successful clinical study should use S. cumini seeds, seed kernels or fruit from India in fairly high doses. Reductions on blood sugar levels by about 30% seem reasonably to be expected. Adverse effects to be expected comprise gastrointestinal disturbances.14
Study shows that S. cumini seed extracts reduce tissue damage in diabetic rat brain.15
Treatment with 400 mg per day of aqueous extracts of Momordica charantia (MC) and Eugenia jambolana (EJ) for 15 days substantially prevented hyperglycemia and hyperinsulinemia induced by a diet high in fructose (63.52+/-2.9 and 66.46+/-2.2 vs. 75.46+/-2.4, respectively).16
The oral antihyperglycemic effect of the water and ethanolic extracts of the fruit-pulp of Eugenia jambolana (EJ) was investigated in alloxan-induced diabetic with fasting blood glucose between 120 and 250 mg/dl as well as severely diabetic rabbits (fasting blood glucose above 250 mg/dl). Water extract was found to be more effective than the ethanolic extract in reducing fasting blood glucose and improving blood glucose in glucose tolerance test.
After treatment of diabetic and severely diabetic rabbits daily once with 25mg/kg, body weight with F-III for 7 and 15 days, respectively, there was fall in fasting blood glucose (38% diabetic; 48% severely diabetic) and improvement in blood glucose during glucose tolerance test (48%) in diabetic rabbits.


Deep Foods – Frozen Jamun Fruit

Jamun Powder (Syzygium cumini)

Vedic Juices Organic Jamun Indian BlackBerry Juice 1 Liter 12 Packs

Basic Ayurveda – Jamun Juice


Chinese Herbal Decoction Ge-Gen-Qin-Lian: An Effective Treatment for Type 2 Diabetes

A Traditional Chinese Medicine (TCM) herbal formula that has been used for the treatment of type-2 diabetes, and which has been documented based on clinical trials, is the Ge-Gen-Qin-Lian decoction (GGQLD).

A number of recent studies from 2011 and 2015 have showed that GGQLD had good clinical effects on type-2 diabetes and the anti-diabetic activities of GGQLD in vivo and in vitro were investigated.  1  2 

GGQLD consists of four herbs:

  • Puerariae Lobatae radix (Ge-Gen) as the principle herb
  • Scutellariae radix (Huang-Qin)
  • Coptidis rhizoma (Huang-Lian)
  • Glycyrrhizae Radix et Rhizoma Praeparata cum Melle (Gan-Cao)

Each of these 4 herbs have primary bioactive compounds that are effective in treating and reducing blood glucose level.  The primary bioactive compounds from these 4 herbs and their effect include:


Puerarin from Ge-Gen reduced blood sugar in diabetic mice, and improved insulin resistance and hyperlipidemia in rats  3 


Baicalin from Huang-Qin had antihyperglycemic effects on diabetic rats  4 


Berberine from Huang-Lian lowered blood glucose significantly by increasing insulin receptor expression  5


Amorfrutins from Gan-Cao have potent antidiabetic activity  6 

Another key component of GGQLD that has been identified called 4-Hydroxymephenytoin is involved in the antidiabetic ingredients of GGQLD stimulating endogenous insulin secretion and ameliorating insulin resistance in 3T3-L1-based insulin resistance models.  7

The Table below lists the antidibetic ingredients in Ge-Gen-Qin-Lian:  (Source) 

Potential antidiabetic ingredients in Ge-Gen-Qin-Lian formula by network target analysis.
Ingredients Herbs CID Literature evidence
4-Hydroxymephenytoin Ge-Gen 119507 /
1-OCTEN-3-OL Ge-Gen 18827 [50]
Berbericinine Huang-Lian 19009 /
Berberine bisulfate Huang-Lian 12457 [51]
Columbamine Huang-Lian 72310 [52]
Coptisine Huang-Lian 72322 [53]
Epiberberine Huang-Lian 160876 [54, 55]
Jatrorrhizine Huang-Lian 72323 [55, 56]
Oxyberberine Huang-Lian 11066 [57]
Dehydrocheilanthifoline Huang-Lian 3084708 [58]
Berberine Huang-Lian 2353 [59]
Indole Huang-Qin 798 [60]
1,3-Diphenylbenzene Huang-Qin 7076 /
2-Formylpyrrole Huang-Qin 13854 /
Guaifenesin Huang-Qin 3516 [61]
1-(1H-Pyrrol-2-yl)ethanone Gan-Cao 14079 [62]
2-Acetyl-1-methylpyrrole Gan-Cao 61240 [63]
m-Ethylphenyl acetate Gan-Cao 76462 /
5,6,7,8-Tetrahydro-4-methylquinoline Gan-Cao 185667 /
/: no evidence.

Sulforaphane Improves Glucose Control

A recently published study on 14 June 2017 in the journal Science Translational Medicine entitled, “Sulforaphane reduces hepatic glucose production and improves glucose control in patients with type 2 diabetes”, found that sulforaphane-containing broccoli sprout extract was well tolerated and improved fasting glucose in human patients with obesity and dysregulated type 2 diabetes.  1 

The authors of the study analyzed the pattern of gene expression associated with type 2 diabetes and compared it to the gene signatures for thousands of drug candidates to find compounds that could counteract the effects of diabetes. By interrogating a library of 3800 drug signatures, the leading candidate from this analysis was sulforaphane, a natural compound found in broccoli,broccoli sprouts, brussel sprouts and other vegetables.

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Figure 1.  Sulforaphane molecule

The authors showed that sulforaphane inhibits glucose production in cultured cells by activating nuclear translocation of nuclear factor erythroid 2–related factor 2 (NRF2) and improves glucose tolerance in rodents on high-fat or high-fructose diets.  It also decreased expression of key enzymes in gluconeogenesis.

Moreover, sulforaphane reversed the disease signature in the livers from diabetic animals and attenuated exaggerated glucose production and glucose intolerance by a magnitude similar to that of the drug metformin.

Finally, sulforaphane, provided as concentrated broccoli sprout extract, reduced fasting blood glucose and glycated hemoglobin (HbA1c) in obese patients with dysregulated type 2 diabetes.


Summary of Benefits of Sulforaphane in Type 2 Diabetes

  • Inhibits glucose production by activating NRF2
  • Improves glucose tolerance
  • Decreased expression of key enzymes in gluconeogenesis
  • Reduced fasting blood glucose
  • Reduced glycated hemoglobin (HbA1c)

Related article:  Broccoli Sprouts and the Health Benefits of Sulforphane

Gymnema sylvestre Improves the Function of and Regenerates Pancreatic Beta Cells

The pancreas is a glandular organ in the digestive system located in the abdominal cavity behind the stomach. It serves as an endocrine gland producing several important hormones that circulate in the blood, including:

  • insulin (important in the metabolism of glucose)
  • glucagon
  • somatostatin
  • pancreatic polypeptide

The pancreas also secretes pancreatic juice containing digestive enzymes that assist digestion and absorption of nutrients in the small intestine.

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Figure 1.  Location of the pancreas  (Source)

The region of the pancreas that contain its endocrine (hormone producing) cells is called the pancreatic islets or islets of Langerhans.  The pancreatic islets constitute 1 to 2% of the pancreas volume and receive 10–15% of its blood flow.

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Figure 2.  Islets of Langerhans  (Source)

A type of cell found in the pancreatic islets are Beta cells.  They make up 65-80% of the cells in the islets.  The primary function of a beta cell is to store and release insulin. Insulin is a hormone that brings about effects which reduce blood glucose concentration.

Image result for beta cells

Figure 3.  Beta-cells of the pancreas  (Source)

The functions of the beta cells can become compromised with insulin resistance and the pathogenesis of diabetes.  Beta cell dysfunction results from inadequate glucose sensing to stimulate insulin secretion and therefore elevated glucose concentrations prevail.

Persistently elevated glucose concentrations above the physiological range result in the manifestation of hyperglycemia. With systemic insulin resistance, insulin signaling within glucose recipient tissues is defective therefore hyperglycemia perseveres.

Image result for beta cell dysfunction

Figure 4.  Potential mechanism of beta-cell failure  (Source)

Beta cell dysfunction supersedes insulin resistance in inducing diabetes. Both pathological states influence each other and presumably synergistically exacerbate diabetes.

Preserving beta cell function and insulin signaling in beta cells and insulin signaling in the glucose recipient tissues will maintain glucose homeostasis.   1

Plant-derived Natural Compounds that Inhance the Functionality of Pancreatic Beta Cells

There is a wide selection of published data on the effects of various plant-derived natural compounds on the functionality of pancreatic beta cells. These natural compounds have been found to directly:

  • enhance insulin secretion
  • prevent pancreatic beta cell apoptosis
  • modulate pancreatic beta cell differentiation and proliferation
  • regenerate pancreatic beta cells

Certain bio-active compounds of plants have confirmed anti-diabetic properties.  Table 1 below lists these botanical plants and their active compounds:

Table 1: Biological functions of plants (bio-active compounds) with confirmed anti-diabetic properties.



Botanical name Active


Anoectochilus roxburghii Kinsenoside Increases pancreatic beta cell regeneration [98]
Biden pilosa 3-β-D-Glucopyranosyl-1-hydroxy-6(E)-tetradecene-8,10,12-triyne
Increases insulin production
Enhances insulin
Camellia sinensis Epigallocatechin-3-gallate Enhances insulin secretion
Inhibits pancreatic beta
cell apoptosis
Capsicum annuum Capsaicin Enhances insulin secretion [1719]
Carica papaya Flavonoids/alkaloids/saponin/tannins Enhances insulin secretion [20, 21]
Curcuma longa Curcumin Enhances insulin secretion [7177]
Ervatamia microphylla Conophylline Induces differentiation into insulin producing
Glycine max Genistein Enhances insulin secretion
Inhibits pancreatic beta
cell apoptosis
Gymnema sylvestre Gymnemic acids Enhances insulin secretion [2232]
Momordica charantia Momordicin Increases pancreatic beta cell regeneration [3343]
Nymphaea stellate Nymphayol Enhances insulin secretion [4446]
Panax ginseng Ginsenoside Enhances insulin secretion
Rhizoma coptidis Berberine Enhances insulin secretion [5863]
Silybum marianum Silymarin Inhibits pancreatic beta cell apoptosis [113118]
Commonly found in plants Resveratrol Inhibits pancreatic beta cell apoptosis [106112]
Commonly found in plants Quercetin Enhances insulin secretion
Inhibits pancreatic beta
cell apoptosis


Source:  Plant-Derived Compounds Targeting Pancreatic Beta Cells for the Treatment of Diabetes


Image result for Plant-Derived Compounds Targeting Pancreatic Beta Cells for the Treatment of Diabetes

Figure 5.  Biological functions of plants (bioactive compounds) with confirmed antidiabetic properties  (Source) (Click on image to enlarge)

Gymnema sylvestre increases pancreatic beta cell regeneration and insulin secretion

Gymnema sylvestre (G. sylvestre) has traditionally been used to treat diabetes in India for centuries and has been an integral part of Ayruvedic medicine.

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Figure 6.  Gymnema sylvestre plant and flowers

The bio-active compound of G. sylvestre are triterpenoid saponins.  The main triterpenoid saponin is gymnemic acids and are considered to be the active compounds responsible for the anti-diabetic effects of G. sylvestre.

G. sylvestre extract is known to stimulate insulin secretion in various pancreatic beta cell lines.  It also has showed hypoglycemic effects via the increase in pancreatic beta cell regeneration and insulin secretion.

The many antidiabetic effects of G. sylvestre include:

  • Decreased plasma glucose levels and significantly induced insulin secretion compared with that in control mice.  2
  • Lowered blood glucose levels through the regeneration of pancreatic beta cells.  3
  • Lowered blood glucose levels in type 2 diabetes patients by increasing insulin secretion.  4
  • Induced significant increases in circulating insulin and C-peptide concomitant with a significant reduction in blood glucose levels.  5 
  • Blood glucose homeostasis through increased serum insulin levels provided by repair/regeneration of the pancreas.  6

Chinese Succulent Plant Shilianhua Regulates Glucose Metabolism and Insulin Sensitivity by Inhibiting GSK-3β and NF-κB

There are a number of recognized ‘blue zones’ around the world which are considered longevity hotspots where a certain amount of the population have long average life spans and a high number of centenarians.

One such blue zone is found in Western China on the slopes of the Himalayas called Bama Yao Autonomous County (aka Bama County):

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Figure 1.  Bama Yao Autonomous County

Bama County is a county in Guangxi, China and is under the administration of Hechi City.

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Figure 2.  Location of Bama Yao Autonomous County

Out of an approximate population of 230,000, Bama County has at least 79 men and women over 100 years old and still very physically active.  Their ratio of 3.52 centenarians per 10,000 people is the highest found anywhere in the world.  It is claimed that the residents of Bama County have the longest average life span of any other country in the world.

Centenarians say age is just a number

Figure 3.  Centenarian resident of Bama County

Among the many environmental factors attributed to blue zones, certain foods and diet play a significant role.  In the case of Bama County, a specific and unique food has been found to play a key role in the longevity of their residents.

A majority of the residents of Bama County consume daily a plant food called Shilianhua or “rock lotus’.  The botanical name of shilianhua is Sinocrassula and is a genus of succulent, subtropical plants of the family Crassulaceae.

The name “Sinocrassula” means “Chinese crassula” and is grown primarily in the province of Yunnan in the south of China, and also from the north of Burma. It grows at an altitude between 2,500 and 2,700 meters and typically blooms from June through August in the Northern Hemisphere. 

Image result for Sinocrassula indica

Figure 4.  Sinocrassula indica, aka Shilianhua or rock lotus

The Pennington Biomedical Research Center, Louisiana State University System; and the Medicinal Plant Research Laboratory, School of Renewable Natural Resources, Louisiana State University Agricultural Center in Baton Rouge, Louisiana, published on 7 April 2009 in the American Journal of Physiology-Endocrinology and Metabolism a paper which examined the anti-diabetes effects of extracts of Shilianhua (SLH).  1

In this study, the researchers isolated the bioactive ingredients of SLH and explored the mechanisms of action of its F100 fraction. The result of the study suggests that the F100 fraction of SLH exhibited a significant activity in enhancing insulin sensitivity in mice.

After treatment with SLH for 8 weeks, fasting insulin and fasting blood glucose (FBG) were reduced by 43 and 27%, respectively.

Glucose consumption was induced significantly by F100 in 3T3-L1 adipocytes, L6 myotubes, and H4IIE hepatocytes in the absence of insulin. F100 also increased insulin-stimulated glucose consumption in L6 myotubes and H4IIE hepatocytes. It increased insulin-independent glucose uptake in 3T3-L1 adipocytes and insulin-dependent glucose uptake in L6 cells. The glucose transporter-1 (GLUT1) protein was induced in 3T3-L1 cells, and the GLUT4 protein was induced in L6 cells by F100.

The data suggest that F100 can act in an insulin- independent manner to stimulate glucose utilization.  F100 may use the insulin-signaling pathway to enhance the glucose consumption.

These results suggest that F100 induces glucose consumption in adipocytes, muscle cells, and hepatocytes in a dose-dependent manner. It may promote insulin activity in cell type-dependent manner (myotubes and hepatocytes). 

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Figure 5.  Effects of F100 in the KK.Cg-Ay/+ diabetic mice. A: effects of F100 on body weight, fat content, food intake, and serum insulin of KK.Cg-Ay/+ mice (n = 9). B: effect of F100 on fasting blood glucose (FBG) of the mice. C: effects of F100 on insulin tolerance of the mice (n = 9). AUC, area under the curve in the insulin tolerance test. Compared with control: *P < 0.05.  (Source)

SLH’s significant activity in enhancing insulin sensitivity in mice may be related to the inhibition by the F100 fraction in SLH of:

  • Glycogen Synthase Kinase-3 Enzyme (GSK-3) (specifcially  (GSK-3β)
  • Nuclear factor kappa-light-chain-enhancer of activated B cells  (NF-κB)

Glycogen Synthase Kinase-3 Enzyme (GSK-3)

Glycogen Synthase Kinase-3 Enzyme (GSK-3) is an enzyme in the body that, when normally activated, is part of the system regulating glucose metabolism.

However, when GSK-3 is overly and excessively activated, it tends to damage cellular structures.  Excessively activated GSK-3 can result in the following health issues in the body:  2 3 4

  • Accelerates aging in heart and muscle
  • Accelerates aging in the skeletal system
  • Accelerates aging in the stomach and liver
  • Develops type II diabetes
  • Develops Alzheimer’s disease  5
  • Impairs autophagy which clears toxic debris inside cells
  • Increases pro-inflammatory cytokines

Glycogen Synthase Kinase-3 Enzyme (GSK-3) Contributes to Alzheimer’s disease

The structural changes and defects that occur in the aging brain which develops into dementia and eventually Alzheimer’s disease include accumulation of beta amyloid plaque and damaged tau proteins.  Both of these results in neurofibrillary tangles which lead to neuron death.

Increased or aberrant over-expressive activity of the GSK-3 enzyme is a contributing factor in these structural changes.

Excessive GSK-3 damages (through the process of the hyperphosphorylation of tau proteins) tau proteins and is thought to directly promote amyloid beta production which leads to neurofibrillary tangles.  6

As mentioned, GSK-3 normally regulates glucose/insulin metabolism.  However, excessive GSK-3 may increase the development of Type II diabetes with glucose impairment and insulin resistance.  It is clear that Type II diabetes increases accumulations of beta amyloid and damaged tau proteins.  7

Because of this correlation, Alzheimer’s disease is often called Type III diabetes.

This conclusion lead to the Alzheimer’s strategy of inhibiting GSK-3 as a means to effectively lower blood glucose, while increasing insulin sensitivity.  8

GSK-3 Inhibitors

Targeted inhibition of GSK-3 may have therapeutic effects with regards to mild cognitive impairment and dementia (including Alzheimer’s disease).  The identified GSK-3 inhibitors are of diverse chemotypes and mechanisms of action, which include inhibitors isolated from natural sources, cations (minerals), and synthetic small molecules.

Shilianhua as a GSK-3 Inhibitor

GSK-3 inhibitors have been reported to improve insulin sensitivity in cellular and animal models.  9  GSK-3β may be a target of F100 in insulin sensitization.

The inhibition of GSK-3 leads to an increase in glycogen synthesis, which promotes insulin sensitivity. The activation of GSK-3 leads to reduction in glycogen synthesis and decrease in insulin sensitivity.

In response to insulin, the enzyme activity of GSK-3 is inhibited through Akt-mediated phosphorylation. The researchers suggested that this inhibitory mechanism may be used by F100 to stimulate glucose uptake in the cellular models and increase insulin sensitivity in mice.

Nuclear factor kappa-light-chain-enhancer of activated B cells  (NF-κB)

NF-κB is a protein complex that controls transcription of DNA, cytokine production and cell survival. NF-κB is found in almost all animal cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, heavy metals, ultraviolet irradiation, oxidized LDL, and bacterial or viral antigens.

NF-κB has long been considered a prototypical pro-inflammatory signaling pathway, largely based on the activation of NF-κB by pro-inflammatory cytokines such as interleukin 1 (IL-1) and tumor necrosis factor α (TNFα), and the role of NF-κB in the expression of other pro-inflammatory genes including cytokines, chemokines, and adhesion molecules

NF-κB is found to be chronically active in many inflammatory diseases, such as:

  • inflammatory bowel disease
  • arthritis
  • sepsis
  • gastritis
  • asthma
  • atherosclerosis

NF-κB has long been considered the “holy grail” as a target for new anti-inflammatory substances, both nutraceutical and pharmaceutical.

In this study the researchers found that NF-κB was strongly inhibited by the F100 fraction in SLH.  Inhibition of inflammation may also contribute to the insulin sensitization by F100. In response to F100, the LPS-induced cytokine (TNFα and MCP-1) expression was reduced in RAW 264.7 macrophages.

The NF-κB inhibition may be a result of GSK-3β suppression by F100.

In conclusion, the researchers stated:

“In summary, we conclude that F100 is a bioactive component in SLH and able to regulate glucose metabolism and insulin sensitivity in mice and in cells. The data suggest that the activity of F100 may be related to the inhibition of GSK-3β. The inhibition may improve insulin signaling in cell. Indirectly, F100 may protect insulin sensitivity by inhibition of NF-κB activity.”  10

U.S. Patents on Shilianhua

Two U.S. Patents have been filed on the medicinal use of Shilianhua, one on June 5, 1999 and the other on October 5, 2006:

US 5911993 A  Homeopathic antidiabetic treatment

A highly effective pure, natural, ingestible antidiabetic may be made from Shilianhua (Echevaria glauca, Sinocrassula berger, Crassulaceae) by washing leaves and/or stems of the Shilianhua plant, crushing them in a grinder, breaking the cell walls to form a filterable material, filtering the material to produce a filtrate, and decompressing and concentrating the filtrate to produce a concentrated solution.

Treatment of, or to prevent, diabetes by lowering blood sugar at least 10% (e. g. about 50%) is practiced by daily administration of about 50-100 mg of powdered extract of Echevaria glauca, Sinocrassula berger, Crassulaceae, or about 20-40 mg of concentrated powdered extract of Echevaria glauca, Sinocrassula berger, Crassulaceae.
WO 2006105407 A1  Medical uses of shilianhua

Shilianhua (SLH) extract has been discovered to display bioactivity in the regulation of fatty acid and glucose metabolism, and in inhibition of an inflammatory response. In addition, an active fraction of SLH extract has been characterized. An active SLH extract protected against insulin resistance through multiple mechanisms, including inhibition of IKK/NF-κB, stimulation of adiponectin secretion, promotion of fatty acid oxidation, and activation of p38.

SLH can be used in the prevention and treatment of diseases in which insulin resistance plays a major role, which includes hyperglycemia, cardiovascular diseases (such as hypertension, heart disease), stroke, renal failure, blindness, and non-traumatic limb amputation. SLH can be used to treat obesity and hyperlipidemia-related diseases by promotion of fatty acid oxidation and energy expenditure. SLH extracts may be used for prevention and treatment of inflammation and oxidative stress, and other diseases in which NF-κB plays a major role, such as arthritis, aging and cancer.  

Phloridzin Effectively Inhibits Glucose Uptake and Traps Advanced Glycation End Products (AGEs)

Phloridzin, also known as Phlorizin, is a glucoside of phloretin, a dihydrochalcone, in the family of bicyclic flavonoids.  It is chemically known as phloretin-2′-β-D-glucopyranoside. 

Phloridzin is primarily found in the skins of apples, in particular, the Malus species.  It is also found in the leaves, bark and seeds of the Malus species.

Phloridzin has been shown to be very effective against glycation and advanced glycation end products (AGEs).  Glycation is considered a main factor in the aging process, which is irreversible when it occurs but can be controlled by diet and supplementation. 

Glycation can form either outside the body through various cooking methods of certain foods and/or inside the body by certain chemical metabolic reactions.  Glycation that occurs outside the body is called exogenous glycation and glycation occuring inside the body is called endogenous glycation. 

Endogenous glycation is the chemical result of the bonding of a sugar molecule with a protein or lipid molecule that produces nonfunctioning and deformed molecules known as advanced glycation end products (AGEs).

Figure 1.  Formation of AGEs  (Source: Glycation and ageing: measurement and treatment from Prime-Journal)

AGEs that stem from a glycation reaction, produces cells that are stiffer and less pliable and more subject to damage and premature aging. When glycated proteins fuse together, this is known as cross-linking. The skin, eyes and heart are particular organs subject to cross-linking.

Exogenous glycation occurs when AGEs are formed by heating proteins and lipids with sugar. Certain forms of cooking can accelerate the exogenous glycation process, such as grilling and frying.

Figure 2. AGEs  (Source: Glycation and ageing: measurement and treatment from Prime-Journal)

AGEs have a range of pathological effects, such as:

  • Increased vascular permeability.
  • Oxidizing LDL.
  • Binding cells—including macrophage, endothelial, and mesangial—to induce the secretion of a variety of cytokines – promoting chronic inflammation.
  • Inhibition of vascular dilation by interfering with nitric oxide.
  • Enhanced oxidative stress – free radicals.

Once an AGE is produced through the endogenous glycation process, it is irreversible. It is therefore important to seek ways to prevent glycation, both endogenously and exogenously.

Mechanism of Phloridzin Against Endogenous Glycation

Phloridzin attacks endogenous glycation in two steps. 

First, phloridzin inhibits glucose uptake by 52%.  1  It inhibits glucose from attaching to the lining cells of the intestine and then blocks the active transport of some, but not all, glucose out of those intestinal lining cells into the bloodstream.  2  3

Second, the glucose that is transported to the bloodstream is responsible for the formation of the dangerous carbonyl molecules that react with proteins and DNA to form AGEs.  4

The formation of these AGEs are prevented by phloridzin by trapping the remaining AGEs that are generated.  This lessens the chain reaction that can occur with AGEs detrimentally reacting with other molecules in the body.  5

In an important study from 2008, researchers found that both phloretin and its glucoside, phloridzin, could efficiently trap certain reactive AGEs called MGO and GO, under physiological conditions.

More than 80% MGO was trapped within 10 min, and 68% GO was trapped within 24 h by phloretin. Phloridzin also had strong trapping efficiency by quenching more than 70% MGO and 60% GO within 24 h. 

This study suggests that dietary flavonoids that have the same A ring structure as phloretin may have the potential to trap reactive dicarbonyl species and therefore inhibit the formation of AGEs.   6  

Berberine exerts a hypoglycemic effect

Berberine is a type of Isoquinoline Alkaloid.

It is found in such plants as Berberis [e.g. Berberis aquifolium (Oregon grape), Berberis vulgaris (barberry), Berberis aristata (tree turmeric)], Hydrastis canadensis (goldenseal), Xanthorhiza simplicissima (yellowroot), Phellodendron amurense (Amur cork tree), Coptis chinensis (Chinese goldthread), Tinospora cordifolia, Argemone mexicana (prickly poppy), and Eschscholzia californica (Californian poppy).

Berberine exerts a hypoglycemic effect, but the mechanism remains unknown. In a study at the Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China, the effect of berberine on glucose uptake was characterized in 3T3-L1 adipocytes. It was revealed that berberine stimulated glucose uptake in 3T3-L1 adipocytes in a dose- and time-dependent manner with the maximal effect at 12 hours. Glucose uptake was increased by berberine in 3T3-L1 preadipocytes as well. Berberine-stimulated glucose uptake was additive to that of insulin in 3T3-L1 adipocytes, even at the maximal effective concentrations of both components.

Unlike insulin, the effect of berberine on glucose uptake was insensitive to wortmannin, an inhibitor of phosphatidylinositol 3-kinase, and SB203580, an inhibitor of p38 mitogen-activated protein kinase. Berberine activated extracellular signal-regulated kinase (ERK) 1/2, but PD98059, an ERK kinase inhibitor, only decreased berberine-stimulated glucose uptake by 32%. Berberine did not induce Ser473 phosphorylation of Akt nor enhance insulin-induced phosphorylation of Akt.

Meanwhile, the expression and cellular localization of glucose transporter 4 (GLUT4) were not altered by berberine. Berberine did not increase GLUT1 gene expression. However, genistein, a tyrosine kinase inhibitor, completely blocked berberine-stimulated glucose uptake in 3T3-L1 adipocytes and preadipocytes, suggesting that berberine may induce glucose transport via increasing GLUT1 activity.

In addition, berberine increased adenosine monophosphate-activated protein kinase and acetyl-coenzyme A carboxylase phosphorylation. These findings suggest that berberine increases glucose uptake through a mechanism distinct from insulin, and activated adenosine monophosphate-activated protein kinase seems to be involved in the metabolic effect of berberine. [1]


[1] Zhou, L., et al. Berberine stimulates glucose transport through a mechanism distinct from insulin. Metabolism. 56(3):405-412, 2007.

Zhang Y, Li X, Zou D et al. (July 2008). “Treatment of type 2 diabetes and dyslipidemia with the natural plant alkaloid berberine”. The Journal of Clinical Endocrinology and Metabolism 93 (7): 2559–65.

Yin J, Xing H, Ye J (May 2008). “Efficacy of berberine in patients with type 2 diabetes mellitus”. Metabolism: Clinical and Experimental 57 (5): 712–7.

Wu LY, Ma ZM, Fan XL et al. (November 2009). “The anti-necrosis role of hypoxic preconditioning after acute anoxia is mediated by aldose reductase and sorbitol pathway in PC12 cells”. Cell Stress & Chaperones 15 (4): 387–94.

Yin J, Gao Z, Liu D, Liu Z, Ye J (January 2008). “Berberine improves glucose metabolism through induction of glycolysis”. American Journal of Physiology. Endocrinology and Metabolism 294 (1): E148–56.

Kong WJ, Zhang H, Song DQ et al. (January 2009). “Berberine reduces insulin resistance through protein kinase C-dependent up-regulation of insulin receptor expression”. Metabolism 58 (1): 109–19. 

Informational References:

Clinical Applications for Berberine

The Berberine Story Gets Better and Better (Life Enhancement July 2013)

Take This Dye for Diabetes From the ancient Silk Road to the modern nutritional pharmacopeia (By Will Block, Life Enhancement November 2010)


Dr. Whittaker – Berberine (500mg)

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Taurine is considered a Wonder Molecule

Taurine’s benefits are very broad and extensive and scientists have described it as a “wonder molecule”.

The often quoted benefits of taurine is that it promotes cardiovascular health, insulin sensitivity, electrolyte balance, hearing function, and immune modulation.

However, it also has the ability to provide protection against reactive carbonyl species and advanced glycation end products (AGE’s).

In a 2004 study at the Department of Biochemistry, Faculty of Science, Annamalai University, Tamil Nadu, India, scientists, Nandhini AT, Thirunavukkarasu V, and Anuradha CV, fed rats a high fructose diet (60% total calories) and then provided a 2% taurine solution for 30 days in order to investigate the antiglycating effect of taurine in high fructose fed rats in vivo and the inhibiting potency of taurine in the process of in vitro glycation.

As a result of the experiment, the contents of glucose, glycated protein, glycosylated haemoglobin and fructosamine were significantly lowered by taurine treatment to high fructose rats. Taurine prevented in vitro glycation and the accumulation of AGEs.

Their conclusion was that these results underline the potential use of taurine as a therapeutic supplement for the prevention of diabetic pathology.


Stimulation of glucose utilization and inhibition of protein glycation and AGE products by taurine

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Caiapo Sweet Potato (Ipomoea batatas) Shows Beneficial Effects of Improving Insulin Resistance

The Caiapo sweet potato is a potato variety of the species Ipomoea batatas, and is native to South America, in particular Brazil.  The potato is a white-skinned sweet potato and the dried powder from the potato has been used traditionally as a natural healthy food.

The name Caiapo is dervied from the Kayapo or Caiapó people, a tribe of people that are indigenous to Brazil.   The Caiapó live in the plain islands of the Mato Grosso and Pará in Brazil, south of the Amazon Basin and along Rio Xingu.  1 

Indios Caiapos

There have been a number of studies from 2002 to 2011 that demonstrate the ability of Caiapo (powder) improve glycemic control by reducing insulin resistance.  It is especially beneficial from the conclusion of these studies to reduce fasting blood glucose levels and reduce HbA1c levels.  HbA1c is also known as glycated hemoglobin and is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over prolonged periods.

The four of the most important research studies on the benefits of Caiapo are summarized below:

Study 1  (January 2002)

Recently, it has been shown that caiapo, the extract of white-skinned sweet potato (Ipomoea batatas), improves glycemic control in rodents by reducing insulin resistance. The aim of our study was to assess the effect of caiapo on glucose metabolism and its tolerability and mode of action in male Caucasian type 2 diabetic patients in a randomized, double-blind prospective study in parallel groups controlled with placebo.

This pilot study demonstrates that ingestion of 4 g caiapo/day for 6 weeks reduces fasting blood glucose and total as well as LDL cholesterol in male Caucasian type 2 diabetic patients previously treated by diet alone. The improvement of insulin sensitivity in the FSIGT indicates that caiapo exerts its beneficial effects via reducing insulin resistance. The treatment was well tolerated, with no apparent side effects.

Table 1—Metabolic parameters before (upper line) and after (lower line) treatment with caiapo in the single groups

Placebo Low dose High dose
n 6 6 6
Fasting plasma glucose (mmol/l) 8.2 ± 0.2 8.8 ± 0.4 8.3 ± 0.6
8.4 ± 0.3 8.4 ± 1.1 7.2 ± 0.4*
Fasting plasma insulin (pmol/l) 8.7 ± 1.7 8.3 ± 1.6 13.4 ± 2.5
8.7 ± 1.2 9.0 ± 1.8 13.2 ± 2.5
Total cholesterol (mmol/l) 5.69 ± 0.23 6.05 ± 0.31 4.97 ± 0.21
5.66 ± 0.31 5.68 ± 0.34 4.45 ± 0.18*
LDL cholesterol (mmol/l) 3.72 ± 0.23 4.11 ± 0.28 3.12 ± 0.16
3.78 ± 0.41 3.80 ± 0.28 2.72 ± 0.16*
HDL cholesterol (mmol/l) 1.40 ± 0.10 1.27 ± 0.10 1.16 ± 0.05
1.42 ± 0.16 1.16 ± 0.10 1.11 ± 0.05
Triglycerides (mmol/l) 1.26 ± 0.15 1.45 ± 0.35 1.52 ± 0.19
1.37 ± 0.30 1.61 ± 0.30 1.33 ± 0.13
HbA1c (%) 7.0 ± 0.3 7.3 ± 0.4 7.1 ± 0.3
7.0 ± 0.2 7.3 ± 0.4 6.8 ± 0.3
Blood pressure (mmHg) 134 ± 13 147 ± 18 135 ± 20
130 ± 18 133 ± 19 128 ± 21
BMI (kg/m2) 28.9 ± 0.9 25.5 ± 0.8 28.6 ± 1.3
29.2 ± 0.8 25.8 ± 0.9 28.1 ± 1.5

In conclusion, this pilot study shows beneficial effects of high-dose caiapo on plasma glucose and total as well as LDL cholesterol levels in patients with type 2 diabetes. These effects relate to a decrease in insulin resistance, as also described in rodents, and were observed without affecting body weight or causing side effects. Therefore, the results of this pilot study indicate that caiapo could potentially play a role in the treatment of type 2 diabetes.  2 

Study 2  (February 2004)

To investigate the tolerability, efficacy, and mode of action of Caiapo, an extract of white sweet potatoes, on metabolic control in type 2 diabetic patients.

A total of 61 type 2 diabetic patients treated by diet were given 4 g Caiapo (n = 30; mean age 55.2 ± 2.1 years; BMI 28.0 ± 0.4 kg/m2) or placebo (n = 31; mean age 55.6 ± 1.5 years; BMI 27.6 ± 0.3 kg/m2) once daily for 12 weeks. Each subject underwent a 75-g oral glucose tolerance test (OGTT) at baseline and after 1, 2, and 3 months to assess 2-h glucose levels.

After treatment with Caiapo, HbA1c decreased significantly (P < 0.001) from 7.21 ± 0.15 to 6.68 ± 0.14%, whereas it remained unchanged (P = 0.23) in subjects given placebo (7.04 ± 0.17 vs. 7.10 ± 0.19%). Fasting blood glucose levels decreased (P < 0.001) in the Caiapo group (143.7 ± 1.9 vs. 128.5 ± 1.7 mg/dl) and did not change in the placebo group (144.3 ± 1.9 vs. 138.2 ± 2.1 mg/dl; P = 0.052).

This study confirms the beneficial effects of Caiapo on plasma glucose as well as cholesterol levels in patients with type 2 diabetes. For the first time, the long-term efficacy of Caiapo on glucose control was demonstrated by the observed decrease in HbA1c. Thus, the neutraceutical Caiapo seems to be a useful agent in the treatment of type 2 diabetes.   3 

Figure 1—

Figure 1— Changes in fasting glucose concentration in the two treatment groups during the study period. Asterisks indicate significant differences for Caiapo versus placebo (*P < 0.05; **P < 0.001). See results for additional statistics.

Figure 2—

Figure 2— Changes in glucose concentration measured 2 h after a 75-g oral glucose load in the two treatments during the study period. Asterisks indicate significant differences for Caiapo versus placebo (*P < 0.005; **P < 0.001). See results for additional statistics.

Study 3  (July 2008)

The extract of the white-skinned sweet potato Ipomoea batatas (Caiapo) has been shown to ameliorate glucose control by improving insulin sensitivity in patients with type 2 diabetes mellitus (T2DM). The present study was designed to further evaluate its mode of action on insulin sensitivity over an extended period of time as well as the effects on fibrinogen and other markers of low-grade inflammation.

In this randomized trial, 27 patients with T2DM on diet only received 4 g of Caiapo daily for 5 months; 34 patients placebo. Before and after therapy, insulin sensitivity [oral glucose insulin sensitivity (OGIS), as glucose clearance from oral glucose tolerance test], parameters of diabetes control, lipids, plasma adiponectin, high-sensitivity C-reactive protein (hs-CRP) and fibrinogen were measured.

This study confirms the beneficial effects of Caiapo on glucose and HbA1c control in patients with T2DM after 5 months follow-up. Improvement of insulin sensitivity was accompanied by increased levels of adiponectin and a decrease in fibrinogen. Thus, Caiapo can be considered as natural insulin sensitizer with potential antiatherogenic properties.  4 

Study 4 (March 2011)

Caiapo sweet potato has been found to contain arabinogalactan proteins.  A study from March 2011 examined the effects of an arabinogalactan protein (WSSP-AGP) from Ipomoea batatas L. on hyperglycemia in db/db mice.

An oral glucose tolerance test indicated significantly decreased plasma glucose levels by WSSP-AGP.  Additionally, an insulin tolerance test found improvement in insulin sensitivity due to treatment with WSSP-AGP.

The study’s conclusion suggests that amelioration of insulin resistance by WSSP-AGP causes to lead its hypoglycemic effects.  5 

Informational References:

Fuji-Sangyo Co., Ltd. – Caiapo Potato Powder

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Serum Glucose Control

Nearly four decades ago, Life Extension Foundation emphatically stated that fasting blood glucose should be below 100 (mg/dL). Yet from 1979 to 1997, the medical establishment dictated that one of the criteria for a diagnosis of diabetes was fasting glucose readings of 140 mg/dL or higher on two separate occasions.

In 1997, the medical establishment revised the fasting glucose threshold for a diagnosis of diabetes to 126 mg/dL. In addition, the medical establishment (American Diabetes Association), characterized the so-called impaired fasting glucose threshold level at 110 mg/dL, which was subsequently lowered in 2003 to what Life Extension originally stated, i.e. that no one should have fasting glucose 100 mg/dL or higher.

The problem is that we now know that the optimal fasting glucose ranges are 70-85 mg/dL based upon the totality of the scientific evidence.33

Those with glucose above 85 mg/dL are at increased risk of heart attack.34 This was shown in a study of nearly 2,000 men where fasting blood glucose levels were measured over a 22-year period. The startling results showed that men with fasting glucose over 85 (mg/dL) had a 40% increased risk of death from cardiovascular disease.

The researchers who conducted this study stated “fasting blood glucose values in the upper normal range appears to be an important independent predictor of cardiovascular death in nondiabetic apparently healthy middle-aged men.”34

At a minimum, you want to see your fasting glucose below 86 mg/dL.

Standard laboratory reference ranges allow an upper-limit of fasting glucose of 99 mg/dL. Yet the most effective anti-aging therapy—caloric restriction—lowers fasting glucose levels to the 70-85 mg/dL range.

Recent studies indicate that keeping fasting glucose levels in the range of 70-85 mg/dL and not allowing after-meal glucose levels to spike higher than 40 mg/dL over your fasting value, favorably influences our longevity genes.72

When after-meal glucose levels surge above 140 mg/dL, risks of virtually all degenerative diseases increase.

Remember that you should strive for fasting glucose levels of no greater than 85 mg/dL (optimal range: 70-85 mg/dL). In response to eating, your blood glucose reading should increase no more than 40 mg/dL above your fasting value. This means if your fasting glucose is 80, your after-meal glucose should be no higher than 120 mg/dL.

Source: Life Extension – Glucose: The Silent Killer


33. McGlothin, P, Averill M. Glucose Control: The Sweet Spot in Longevity. The CR Way: Using the Secrets of Calorie Restriction for a Longer, Healthier Life. NY: HarperCollins; 2008:57-78.

34. Bjornholt JV, Erikssen G, Aaser E, et al. Fasting blood glucose: an underestimated risk factor for cardiovascular death. Results from a 22-year follow-up of healthy nondiabetic men. Diabetes Care. 1999 Jan;22(1):45-9.

72. Available at:…/High_Glucose_after_Meals_is…. Accessed August 2, 2010.

73. Available at: Accessed July 29, 2010.

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