Mastic extends benefits that go beyond bugs and insulin

Diabetes and H. Pylori
Intensify Alzheimer’s

Is it possible to hobble three diseases at once?

By Will Block

T he hypothesis that Alzheimer’s disease (AD) is principally a metabolic disease with biochemical features that correspond with diabetes mellitus and other peripheral insulin resistance disorders continues to gather attention.* This is because brain insulin/IGF (insulin glucose factor) resistance and its consequences can account for most of the structural and functional abnormalities in AD.


*We have written about this before (see “Is Alzheimer’s Disease a Type of Diabetes? Proof that the brain produces insulin sheds new and provocative light on a complex question” in the May 2005 issue and “More Evidence that Alzheimer’s Is Type 3 Diabetes: Impaired insulin signaling is linked to reduced acetylcholine levels and thus to cognitive impairment” in the February 2006 issue, for example.)


Alzheimer’s as a Neuroendocrine Disorder

Consequently, AD has been considered to be, at least in part, a neuroendocrine disorder, with some researchers even referring to AD as type 3 diabetes. In the brain, insulin functions by controlling neurotransmitter release processes at the synapses and activating signaling pathways associated with learning and long-term memory. The idea that AD may be a kind of “brain diabetes” is not new—it was proposed by German neuroscientists in the 1990s. It was known that there is a significant decline in glucose metabolism (a hallmark of diabetes) in the brains of Alzheimer’s patients and that enhancing this process by administering glucose or insulin could improve memory and other cognitive functions. It was also known that type 2 diabetes is, in fact, a risk factor for AD. More recently, the converse was discovered: AD predisposes its victims to type 2 diabetes.1

Insulin Resistant Diseases and Alzheimer’s

While AD can occur as a separate disease process, it can also occur in association with systemic insulin resistance diseases, including obesity, diabetes, and even fatty liver disease. Recently, researchers investigating brain metabolic dysfunction at the core of AD have written, “Whether primary or secondary in origin, brain insulin/IGF resistance initiates a cascade of neurodegeneration that is propagated by metabolic dysfunction, increased oxidative and ER stress, neuro-inflammation, impaired cell survival, and dysregulated lipid metabolism.”2 Processes such as these affect brain cell functions, reduce neurotransmitter equilibrium, and cause the formation of toxic Tau proteins and amyloid beta plaque, along with insoluble neurofibrillary tangles that accumulate in the brain.


Consequently, AD has been
considered to be, at least in part, a
neuroendocrine disorder, with some
researchers even referring to AD as
type 3 diabetes.


The net result of promoting these benchmarks of AD is further deterioration due to a harmful feedback loop that progressively worsens the effects of insulin resistance. This leads to the formation of reactive oxygen and reactive nitrogen species that adversely alter lipid, protein, and DNA chemical compounds, which in turn permanently damage basic cellular and molecular functions.

Figure 1. (1) Type 2 diabetes can lead to the induction of insulin resistance in the brain. (2) Reduction of insulin signaling in the brain increases the activities of β secretases and GSK-3β which (3) increase levels of toxic amyloid-beta (Aβ) oligomers, aka amyloid beta-derived diffusible ligands (ADDLs). At the same time, (4) insulin resistance lowers the expression of insulin-degrading enzyme (IDE). (5) Reduced IDE then leads to increased (Aβ) and (6) accumulation of ADDLs. Type 2 diabetes also causes (7) hyperinsulinemia which exacerbates IDE deficiencies because (8) excess insulin occupies IDE binding sites rendering them unavailable for Aβ. The increased amyloidogenic processing that occurs in insulin resistance, combined with decreased Aβ clearance by IDE, results in a deleterious positive-feedback cycle as (9) ADDLs contribute to insulin resistance in the brain. As Aβ levels continue to rise, insulin resistance worsens—leading to further production of the toxic Aβ oligomers.
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Impaired Insulin Signaling and Alzheimer’s

Original research demonstrates that impaired insulin signaling may be incriminated in AD, and post-mortem brain studies show that insulin expression is inversely proportional to what constitutes a takeoff stage for AD progression.3 In this study, researchers also demonstrated that neurotoxins—called amyloid beta-derived diffusible ligands (ADDLs)—interfere with signal transduction at synapses, making the cell insulin resistant (see Fig. 1).

ADDLs create a cascade of problems including: the reduction of synaptic plasticity, the potentiation of synapse loss, oxidative damage, and AD-type tau hyperphosphorylation. Both diabetes and AD increase oxidative stress. They also share the production of advanced glycation end products (AGEs). As pointed out above, diabetics have an increased risk for AD because AGEs accumulate in neurofibrillary tangles and amyloid plaques in AD brains. At the same time, impaired insulin signaling is linked to reduced acetylcholine levels and thus to cognitive impairment.

Better Cognitive Health Through Mastic

Last month’s Life Enhancement featured an article (See “Ulcer Bug Eradication Empowers Galantamine”) showing that mastic gum, by eradicating H. pylori (Hp), could lead the way to better cognitive health and enhance the effectiveness of the acetylcholinesterase inhibitor galantamine, thus improving AD, as well as cognitive function. In the principal study cited, Chinese researchers from Taiwan examined 30,142 patients with both AD and peptic ulcers.4 The researchers discovered that eradication of the patient population’s Hp decreased the risk of AD progression. While the eradication was achieved through the use of drugs—a proton pump inhibitor or H2 receptor blocker, plus clarithromycin or metronidazole, plus amoxicillin or tetracycline, with or without Bismuth—mastic has also been found to be more effective, and without the side effects associated with the drugs.5


In the brain, insulin functions by
controlling neurotransmitter release
processes at the synapses and
activating signaling pathways
associated with learning and
long-term memory.


The drug treatments (called triple and quadruple therapy) can cause multiple side effects (including nausea, vomiting, and diarrhea). Moreover, the antibiotics used (such as clarithromycin) kill beneficial digestive-tract bacteria, and can contribute to the growing problem of antibiotic resistance. Also, the proton pump inhibitor can alter gastric pH and cause other negative consequences. Furthermore, while triple (or quadruple) therapy is usually successful in eliminating the bug from the stomach and intestines within a few weeks, the gastrointestinal (digestive) tract begins at the mouth, not the stomach, and H. pylori commonly infects the mouth as well as parts south.

Eradication of H. Pylori Slows Down Alzheimer’s

Whether or not the bacteria do much damage in the mouth is not clear, yet recent studies raise the possibility that it might increase the risk of oral cancer.6 Even if they didn’t, though, we would still not want to harbor them there, for one simple reason: things in the mouth can go south. That’s why the reinfection rate with H. pylori is relatively high in people who have eradicated the bug in their stomachs and intestines—sooner or later, some of the bacteria in their mouths may migrate down there and take up residence all over again. This is good reason to use an oral form of mastic, such as a chewable wafer.

At the bottom line, eradication of Hp decreases the progression of dementia in AD patients with peptic ulcers.

Better Cardiovascular/Liver Health with Mastic

A recent paper just published in the Journal of Medical Food researchers found that mastic from Chios, Greece confers beneficial cardiovascular and liver protective properties.7 In 12-week-old male mice—chosen because they are susceptible to diet-induced obesity, type 2 diabetes, and atherosclerosis—diabetes was induced by streptozocin, a naturally occurring chemical that is particularly toxic to the insulin-producing beta cells of the pancreas in mammals. These mice were then assigned to three groups: NC, controls; LdM, animals receiving low dose mastic for 8 weeks (20 mg/kg body weight [BW]); and HdM animals receiving high dose mastic (500 mg/kg BW) for the same period. Each group contained 9 mice.


Low-dose mastic resulted in
significantly lower serum glucose,
cholesterol, low-density lipoprotein
cholesterol, and triglyceride levels
and improved high-density lipoprotein
cholesterol levels.


At baseline, 4 weeks, and 8 weeks serum lipid and glucose levels were determined. Serum total protein, adiponectin, and resistin levels were also measured at the end of the experiment. Microscopic examination of the mouse tissues was done in order to study the manifestations of disease. This was performed for liver, kidney, aorta, and heart lesions. After 4 weeks, mastic administration resulted in decreased serum glucose and triglyceride levels in both LdM and HdM. Also, body weight levels were reduced in LdM group compared with controls.

Mastic is Antidiabetic

When the experiment ended at 8 weeks, LdM presented significantly lower serum glucose, cholesterol, low-density lipoprotein cholesterol, and triglyceride levels and improved high-density lipoprotein cholesterol levels compared with control group.

The HdM group had ameliorated serum triglyceride levels and liver steatosis observed in control group was partially reversed in both the LdM and HdM groups. Mastic administered in low dosages improved glucose and lipid disturbances in diabetic mice while alleviating liver damage.

In conclusion, mastic in low dosages appears effective in improving the disturbed glucose and lipid levels of the experimentally diabetic mice. Further, hepatic damage is alleviated during mastic administration. From these results it is possible to conclude that mastic is a potent natural antidiabetic agent.

Mastic is a Dual Weapon Against Alzheimer’s Disease

A recent search in the National Library of Medicine’s PubMed could find no association between mastic and memory (mastic OR mastic gum OR pistacia lentinus OR mastiche OR damha sakiz OR chios OR mastichochoria) AND (arousal OR attention OR consciousness OR decision making OR executive functions OR natural language OR learning OR memory OR motor coordination OR perception OR planning OR problem solving). We’ll have to wait longer for the right study.

Nevertheless, in keeping with the evidence that AD may be a type of diabetes—or at least associated with diabetic injury—accumulated and recent research clearly implies that mastic can play an important role in reducing dementia and AD. Also, because of the research showing its ability to kill the ulcer bug, along with new evidence that eradication of H. pylori appears to make galantamine more effective, what we have in mastic is a twofer.


If you have a metabolic disorder or if
you are developing one, you should
know that you are at significantly
increased risk for cognitive decline
and the development of vascular
dementia and AD.


An Ounce of Prevention …

Obesity, metabolic syndrome, and type 2 diabetes are related disorders with widespread harmful effects throughout the body, including the brain. If you have a metabolic disorder or if you are developing one, you should know that you are at significantly increased risk for cognitive decline and the development of vascular dementia and AD. The same is true for H. pylori. If you have it, get rid of it. Your memory may suffer the consequences if you don’t.

References

  1. Janson J, Laedtke T, Parisi JE, O’Brien P, Petersen RC, Butler PC. Increased risk of type 2 diabetes in Alzheimer disease. Diabetes. 2004;53: 474-81.
  2. de la Monte SM, Tong M. Brain metabolic dysfunction at the core of Alzheimer’s disease. Biochem Pharmacol. 2013 Dec 28. pii: S0006-2952(13)00796-X. doi:10.1016/j.bcp.2013.12.012. [Epub ahead of print]
  3. Steen E, Terry BM, Rivera EJ, et al. Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer’s disease – is this type 3 diabetes? J Alzheimers Dis. 2005;7:63-80.
  4. Chang YP, Chiu GF, Kuo FC, Lai CL, Yang YH, Hu HM, Chang PY, Chen CY, Wu DC, Yu FJ. Eradication of Helicobacter pylori Is Associated with the Progression of Dementia: A Population-Based Study. Gastroenterol Res Pract. 2013;2013:175729. doi: 10.1155/2013/175729. Epub 2013 Nov 25.
  5. Dabos KJ, Sfika E, Vlatta LJ, Giannikopoulos G. The effect of mastic gum on Helicobacter pylori: a randomized pilot study. Phytomedicine. 2010 Mar;17(3-4):296-9. doi: 10.1016/j.phymed.2009.09.010. Epub 2009 Oct 29.
  6. Dayama A, Srivastava V, Shukla M, Singh R, Pandey M. Helicobacter pylori and oral cancer: possible association in a preliminary case control study. Asian Pac J Cancer Prev. 2011;12(5):1333-6.
  7. Georgiadis I, Karatzas T, Korou LM, Agrogiannis G, Vlachos IS, Pantopoulou A, Tzanetakou IP, Katsilambros N, Perrea DN. Evaluation of Chios Mastic Gum on Lipid and Glucose Metabolism in Diabetic Mice. J Med Food. 2014 Jan 9. [Epub ahead of print]


Will Block is the publisher and editorial director of Life Enhancement magazine.

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