Tag Archives: obesity

Is Your Type of Heart Disease Curable of Just Treatable?

Can Your Type of Heart Disease be Cured or Just Treated?

Because of the growing list on the Real Poisoning of America – Glycation, it’s become evident that I need to display a different post for the different types of damage that glycation induces. From atherosclerosis and other heart related diseases, I’ll reserve this notice for that purpose only. All cancer reports will be located on the cancer page.  Dementia will be on a separate post as well with all other diseases and disorders inflammation is responsible for.

The whole premise behind these posts is to prove that the only way you can prevent these horrendous diseases, is to stop the glycation that is responsible for them and the only way you can stop the glycation is to stop feeding it. It’s really a simple solution, just not an easy one because of the addiction factor. However, YOU and only YOU have control over this and it all depends on what YOU put in you mouth when you eat.

I’ll admit that that can be hard when you have a whole industry trying to get you to eat more of what it is that glycates. This is because they are connected to another industry that feeds off of the unsuspected that buy into this ruse, all those whom the glycation affects, the public.                                               Get the whole story!

Listed below from PubMed or PMC or the FDA are reports of studies done on the effects of glycation and its influence in any CVD or disease influenced by inflammation, which is a direct cause of glycation.

Advanced glycation endproducts induce apoptosis of endothelial progenitor cells by activating receptor RAGE and NADPH oxidase/JNK signaling axis.

Elevated levels of advanced glycation endproducts (AGEs) is an important risk factor for atherosclerosis. Dysfunction of endothelial progenitor cells (EPCs), which is essential for re-endothelialization and neovascularization, is a hallmark of atherosclerosis. However, it remains unclear whether and how AGEs acts on EPCs to promote pathogenesis of atherosclerosis. In this study, EPCs were exposed to different concentrations of AGEs. The expression of NADPH and Rac1 was measured to investigate the involvement of NADPH oxidase pathway. ROS was examined to indicate the level of oxidative stress in EPCs. Total JNK and p-JNK were determined by Western blotting. Cell apoptosis was evaluated by both TUNEL staining and flow cytometry. Cell proliferation was measured by (3)H thymidine uptake. The results showed that treatment of EPCs with AGEs increased the levels of ROS in EPCs. Mechanistically, AGEs increased the activity of NADPH oxidase and the expression of Rac1, a major component of NADPH. Importantly, treatment of EPCs with AGEs activated the JNK signaling pathway, which was closely associated with cell apoptosis and inhibition of proliferation. Our results suggest that the RAGE activation by AGEs in EPCs upregulates intracellular ROS levels, which contributes to increased activity of NADPH oxidase and expression of Rac1, thus promoting cellular apoptosis and inhibiting proliferation. Mechanistically, AGEs binding to the receptor RAGE in EPCs is associated with hyperactivity of JNK signaling pathway, which is downstream of ROS. Our findings suggest that dysregulation of the AGEs/RAGE axis in EPCs may promote atherosclerosis and identify the NADPH/ROS/JNK signaling axis as a potential target for therapeutic intervention.

With the list growing past 17,729 studies on the effects of glycation, I think this message about the process of glycation should be wider known. This is the basis of all modern disease. Why has it been kept hidden? Is it due to industrial concerns? What would happen if you wiped 98% of all illness?

This report dictates how the modification of proteins (glycation) is involved in atherosclerosis. Is this the smoking gun that carbs are dangerous foods to eat? Even though this report is from Dec 2016, it only says, again, what hundreds if not thousands of other reports dictate. They all dictate glycation is dangerous. What causes glycation should be avoided at all costs, to ensure optimal health.

Post-translational modification of proteins imparts diversity to protein functions. The process of glycation represents a complex set of pathways that mediates advanced glycation endproduct (AGE) formation, detoxification, intracellular disposition, extracellular release, and induction of signal transduction. These processes modulate the response to hyperglycemia, obesity, aging, inflammation, and renal failure, in which AGE formation and accumulation is facilitated. It has been shown that endogenous anti-AGE protective mechanisms are thwarted in chronic disease, thereby amplifying accumulation and detrimental cellular actions of these species. Atop these considerations, receptor for advanced glycation endproducts (RAGE)-mediated pathways down regulate expression and activity of the key anti-AGE detoxification enzyme, glyoxalase-1 (GLO1), thereby setting in motion an interminable feed-forward loop in which AGE-mediated cellular perturbation is not readily extinguished. In this review, we consider recent work in the field highlighting roles for glycation in obesity and atherosclerosis and discuss emerging strategies to block the adverse consequences of AGEs. This article is part of a Special Issue entitled: The role of post-translational protein modifications on heart and vascular metabolism edited by Jason R.B. Dyck & Jan F.C. Glatz.

This is the smoking gun that proves what glucose consumption does to the body in the form of atherosclerosis. How long before the FDA or the USDA will admit that this is what happens after ingesting grains? Will the Heart Association say anything about this? What about the American Diabetic Association? I wonder if this news will reach any regulatory agency. My guess is if Monsanto has anything to say about it, they’ll say “where’s the money in it.”

This report from Aug 1 1989, reveals how aware we were then, that glycation is a damaging process that is caused by excess glucose in your system. One would think that 27 and a half years would be long enough to reveal this information. Apparently, it isn’t.

We studied 11 diabetic patients, all of whom had severe atherothrombotic disease, and 11 normal controls. Overall glycation was assessed by the extent of incorporation of [3H]-NaBH4 into fructosyl lysine separated from whole platelet proteins following amino acid analysis. Fructosyl lysine represented 5.7% +/- 1.0 S.D. of the total radioactivity in the normal whole platelet samples. Increased glycation was observed in platelets from 5 of the 11 diabetics. Platelet glycation did not correlate with glycation of hemoglobin or albumin. The pattern of glycation of various platelet proteins in whole platelets, as determined by the incorporation of [3H]-NaBH4 into electrophoretically separated proteins did not display selectivity, although myosin and glycoproteins IIb and IIIa showed relatively increased levels of [3H]-NaBH4 incorporation. Artificially glycated platelet membranes exhibited glycation mainly in proteins corresponding to the electrophoretic mobility of myosin, glycoproteins IIb and IIIa.

The previous report was published in 1989 yet have you heard anything about it? Didn’t they have idea, at that time, what carbs were doing to the body, when ingested? I guess they needed more studies. Over 17,000 of them have been filed as of yet. Why has it taken until 2010 to learn any of this? Even today, they still are reluctant to admit such, that carbs are dangerous foods to be eating.

  • Advancedglycation end products: An emerging biomarker for adverse outcome in patients with peripheral artery disease.

Patients with peripheral artery disease (PAD) suffer from widespread atherosclerosis. Partly due to the growing awareness of cardiovascular disease, the incidence of PAD has increased considerably during the past decade. It is anticipated that algorithms to identify high risk patients for cardiovascular events require being updated, making use of novel biomarkers. Advanced glycation end products (AGEs) are moieties formed non-enzymatically on long-lived proteins under influence of glycemic and oxidative stress reactions. We elaborate about the formation and effects of AGEs, and the methods to measure AGEs. Several studies have been performed with AGEs in PAD. In this review, we evaluate the emerging evidence of AGEs as a clinical biomarker for patients with PAD.

Peripheral Artery disease is often the start of Atherosclerosis and all CVDs. They are a direct cause of glycation. Glycation is controllable by controlling the amount of carbs you put in your mouth every time you eat.

This following study shows how your body reacts to the glucose infusion by sending out macrophages to counteract the damage presented by the glucose. The modified LDL particles are the glycated endproducts of what happens to your cholesterol with glucose in your system.

How do macrophages sense modified low-density lipoproteins?

Abstract

In atherosclerosis, serum lipoproteins undergo various chemical modifications that impair their normal function. Modification of low density lipoprotein (LDL) such as oxidation, glycation, carbamylation, glucooxidation, etc. makes LDL particles more proatherogenic. Macrophages are responsible for clearance of modified LDL to prevent cytotoxicity, tissue injury, inflammation, and metabolic disturbances. They develop an advanced sensing arsenal composed of various pattern recognition receptors (PRRs) capable of recognizing and binding foreign or altered-self targets for further inactivation and degradation. Modified LDL can be sensed and taken up by macrophages with a battery of scavenger receptors (SRs), of which SR-A1, CD36, and LOX1 play a major role. However, in atherosclerosis, lipid balance is deregulated that induces inability of macrophages to completely recycle modified LDL and leads to lipid deposition and transformation of macrophages to foam cells. SRs also mediate various pathogenic effects of modified LDL on macrophages through activation of the intracellular signaling network. Other PRRs such Toll-like receptors can also interact with modified LDL and mediate their effects independently or in cooperation with SRs.

What you should think about, is what would happen if the glucose weren’t there. The cholesterol can do what it’s supposed to do, feed your body.

From Dec 2016, Coronary Heart Disease and Ischemic stroke are shown to be influenced by another RAGE Gly82ser. How many more of these do they have to find before they realize that you can prevent this by keeping carbs out of the diet?

Association of RAGE gene Gly82Ser polymorphism with coronary artery disease and ischemic stroke: A systematic review and meta-analysis.

Abstract

BACKGROUND:

The receptor for advanced glycosylation end products (RAGE) has been widely linked to diabetic atherosclerosis, but its effects on coronary artery disease (CAD) and ischemic stroke (IS) remain controversial. The Gly82Ser polymorphism is located in the ligand-binding V domain of RAGE, suggesting a possible influence of this variant on RAGE function. The aim of the present study is to clarify the association between the RAGE Gly82Ser polymorphism and susceptibility to CAD and IS.

CONCLUSIONS:

The current meta-analysis suggests that the RAGE Gly82Ser polymorphism is associated with an increased risk of CAD and IS, especially in the Chinese population. However, better-designed studies with larger sample sizes are needed to validate the results.

The following report submitted Sep 31, 2011 shows the influence of RAGE in VRD ;

RAGE-dependent activation of the onco-protein Pim1 plays a critical role in systemic vascular remodeling processes.

Abstract

OBJECTIVE:

Vascular remodeling diseases (VRD) are mainly characterized by inflammation and a vascular smooth muscle cells (VSMCs) proproliferative and anti-apoptotic phenotype. Recently, the activation of the advanced glycation endproducts receptor (RAGE) has been shown to promote VSMC proliferation and resistance to apoptosis in VRD in a signal transducer and activator of transcription (STAT)3-dependant manner. Interestingly, we previously described in both cancer and VRD that the sustainability of this proproliferative and antiapoptotic phenotype requires activation of the transcription factor NFAT (nuclear factor of activated T-cells). In cancer, NFAT activation is dependent of the oncoprotein provirus integration site for Moloney murine leukemia virus (Pim1), which is regulated by STAT3 and activated in VRD. Therefore, we hypothesized that RAGE/STAT3 activation in VSMC activates Pim1, promoting NFAT and thus VSMC proliferation and resistance to apoptosis. Methods/Results- In vitro, freshly isolated human carotid VSMCs exposed to RAGE activator Nε-(carboxymethyl)lysine (CML) for 48 hours had (1) activated STAT3 (increased P-STAT3/STAT3 ratio and P-STAT3 nuclear translocation); (2) increased STAT3-dependent Pim1 expression resulting in NFATc1 activation; and (3) increased Pim1/NFAT-dependent VSMC proliferation (PCNA, Ki67) and resistance to mitochondrial-dependent apoptosis (TMRM, Annexin V, TUNEL). Similarly to RAGE inhibition (small interfering RNA [siRNA]), Pim1, STAT3 and NFATc1 inhibition (siRNA) reversed these abnormalities in human carotid VSMC. Moreover, carotid artery VSMCs isolated from Pim1 knockout mice were resistant to CML-induced VSMC proliferation and resistance to apoptosis. In vivo, RAGE inhibition decreases STAT3/Pim1/NFAT activation, reversing vascular remodeling in the rat carotid artery-injured model.

CONCLUSIONS:

RAGE activation accounts for many features of VRD including VSMC proliferation and resistance to apoptosis by the activation of STAT3/Pim1/NFAT axis. Molecules aimed to inhibit RAGE could be of a great therapeutic interest for the treatment of VRD.

Advanced glycation end products increase lipids accumulation in macrophages through upregulation of receptor of advanced glycation end products: increasing uptake, esterification and decreasing efflux of cholesterol.

Advanced glycation end products increase lipids accumulation in macrophages through upregulation of receptor of advanced glycation end products: increasing uptake, esterification and decreasing efflux of cholesterol.

BACKGROUND:

Previous reports have suggested that advanced glycation end products (AGEs) participate in the pathogenesis of diabetic macroangiopathy. Our previous study have found that AGEs can increase the lipid droplets accumulation in aortas of diabetic rats, but the current understanding of the mechanisms remains incomplete by which AGEs affect lipids accumulation in macrophages and accelerate atherosclerosis. In this study, we investigated the role of AGEs on lipids accumulation in macrophages and the possible molecular mechanisms including cholesterol influx, esterification and efflux of macrophages.

METHODS:

THP-1 cells were incubated with PMA to differentiate to be macrophages which were treated with AGEs in the concentration of 300 μg/ml and 600 μg/ml with or without anti-RAGE (receptor for AGEs) antibody and then stimulated by oxidized-LDL (oxLDL) or Dil-oxLDL. Lipids accumulation was examined by oil red staining. The cholesterol uptake, esterification and efflux were detected respectively by fluorescence microscope, enzymatic assay kit and fluorescence microplate. Quantitative RT-PCR and Western blot were used to measure expression of the moleculars involved in cholesterol uptake, synthesis/esterification and efflux.

RESULTS:

AGEs increased lipids accumulation in macrophages in a concentration-dependent manner. 600 μg/ml AGEs obviously unregulated oxLDL uptake, increased levels of cholesterol ester in macrophages, and decreased the HDL-mediated cholesterol efflux by regulating the main molecular expression including CD36, Scavenger receptors (SR) A2, HMG-CoA reductase (HMGCR), ACAT1 and ATP-binding cassette transporter G1 (ABCG1). The changes above were inversed when the cells were pretreated with anti-RAGE antibody.

CONCLUSIONS:

The current study suggest that AGEs can increase lipids accumulation in macrophages by regulating cholesterol uptake, esterification and efflux mainly through binding with RAGE, which provide a deep understanding of mechanisms how AGEs accelerating diabetic atherogenesis.

This is the proof that AGEs inhibit proper cell nutrition by preventing the flow of cholesterol into the cell. This allows accumulation of LDL particles in your blood. Usually with a carbohydrate diet, those LDL particles are going to be ApoB particles and those are the most proliferate in all disease. Again, this is something you have full control over, as you don’t have to eat this food. There are plenty of healthier alternatives.

The next study details how glycol-AGEs work their way into the cellular wall of your arteries creating Atherosclerosis. What you should think about is, could this happen without glucose in your system? Can you live without glucose? If you answered YES to both of those questions, you’re on your way to a healthier body.

Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium.

Advanced glycation end-products (AGEs) are involved in the development of vascular smooth muscle cell (VSMC) dysfunction and the progression of atherosclerosis. However, AGEs may indirectly affect VSMCs via AGEs-induced signal transduction between monocytes and human umbilical endothelial cells (HUVECs), rather than having a direct influence. This study was designed to elucidate the signaling pathway underlying AGEs-RAGE axis influence on VSMC dysfunction using a co-culture system with monocytes, HUVECs and VSMCs. AGEs stimulated production of reactive oxygen species and pro-inflammatory mediators such as tumor necrosis factor-α and interleukin-1β via extracellular-signal-regulated kinases phosphorylation and nuclear factor-κB activation in HUVECs. It was observed that AGEs-induced pro-inflammatory cytokines increase VSMC proliferation, inflammation and vascular remodeling in the co-culture system. This result implies that RAGE plays a role in AGEs-induced VSMC dysfunction. We suggest that the regulation of signal transduction via the AGEs-RAGE axis in the endothelium can be a therapeutic target for preventing atherosclerosis.

Do you have any idea of how to regulate the transduction of AGEs? It’s simple, go keto. Will an industry that depends on your illness, tell you that? I seriously doubt it. Since it’s this industry that regulates the regulatory agencies, I doubt that you’ll ever hear it from them. That’s why it’s so important to follow your own advice to stay healthy, stay away from unhealthy substances. Now you know how unhealthy glucose is, simply due to its glycative effects.

Are these enough reports to prove how directly influence diabetes? After reading this can you see the logic in controlling your diabetes by controlling your carb intake? Where are the warnings from the FDA and the USDA? Don’t they care about what they’re recommending? Don’t they understand because of their recommendations, they sending millions of Moms and Dads, sisters and brothers, husbands and wives to their slow, expensive, painful deaths?

These are free reports that are available to everyone. All you have to do is search for them at the National Library of Medicine in the National Institute of Health. There are literally 100s of thousands of reports on the effects of glycation that remain hidden in the PubMed and PMC databases except to the few who look through them.  The only ones looking through this database are the drug companies looking for more ways to make money. Nobody is looking to warn anyone of the dangers of this food.

My question is why? The answer I get is, “there’s no money in it”. That’s is why I said in my first book, it would be a shame if profits and money weren’t the primary motivating factors in our society, but they are, and we have to live with it. That’s why I choose not to buy into it. It’s the same choice you have.

 

 

 

 

Carbs and Cancer go together like love and marriage.

How Carbs Influence Cancer

17601735-cancer-word-cloud-concept-with-great-terms-such-as-disease-chemo-survivor-patient-doctor-and-more
Cancer is responsible for over 8,200,000 deaths every year.

Cancer comes in so many different forms , it makes it very difficult to nail down any one solution for all the different types of cancer. However, playing a major influence in half of the different types of cancer, listed below, is one common thread that permeates our diets everywhere – glucose. It’s woven of three strands – wheat, sugar and grain based foods (flour and sugar). These basic staples that we were all encouraged to eat massive quantities of, is actually what’s killing us. The worst aspect of this whole problem is that we were told to eat them. We were told that they should be the largest portion of our meals and that we eat them on a daily basis. We were told to do this because, (we were told) that it was healthy for us. Why was the truth was never shared? I don’t know. But we do know now, just how dangerous this food staple really is. Cancer is like the carriage to the carbs’ horse. Carbs lead the way and the cancer follows.

I mentioned in Carbs! The Newly Discovered Death Sentence that this is not healthy food, and I intend to prove it, starting with  this page.

Because of the lack of studies done of the effects of wheat in the diet and cancer, it’s not always easy to piece the information together. Many of the studies that were done years ago have been suppressed from public knowledge and are not easy to obtain now. Dr Davis and Dr Perlmutter have already located many of these studies and they can be found in their books, Wheat Belly and Grain Brain. I spent only enough time to decipher sugar and wheat’s influence in half of the various types of cancer listed below. If the CPSC is considering warnings for chemicals that cause cancer, (which they are in California) why isn’t anyone considering warnings for the consumption of these food staples, sugar and flour?

Suffice it to say, there is enough evidence here to prove that this food source should come with the same warning that everything that causes cancer has to bear, like cigarettes, and now, processed meats and fast foods, and chemicals in California. (California’s attorney general, Bill Lockyer, filed suit in August against McDonald’s; Burger King; Frito-Lay, owned by PepsiCo; and six other food companies, saying that they should be forced to put labels on all fries and potato chips sold in California. The proposed warning might say something to this effect: “This product contains a chemical known to the state of California to cause cancer.”)

It’s interesting that California is going after fast food companies for the “cancer causing French fries” when it’s the bread that has as much if not more influence on cancer as trans-fats. I’ll admit, French fries play a definite role in cancer, but if they’d only look at the studies that show how sugar and wheat cause cancer, diabetes, HBP, cardio-vascular disease, digestive disorders, etc they’d soon have labels on everything that flour and sugar were used in. The full list is viewable on the page mentioned above.

This page is going to show how this food actually contributes to the environmental factors that are at the root cause of many cancers.

Cancer – There are over 100 different known cancers that affect humans.[2] causing 8.2 million deaths as of 2012 The great majority of cancers, some 90–95% of cases, are due to environmental factors. The remaining 5–10% are due to inherited genetics.[5] Environmental, as used by cancer researchers, means any cause that is not inherited genetically, such as lifestyle, economic and behavioral factors, and not merely pollution.[28] Common environmental factors that contribute to cancer death include tobacco (25–30%), diet and obesity (30–35%), infections (15–20%), radiation (both ionizing and non-ionizing, up to 10%), stress, lack of physical activity, and environmental pollutants.[5] Diet, physical inactivity, and obesity are related to up to 30–35% of cancer deaths.[5][39  The largest influence in obesity is wheat, sugar and grain based foods.

We’re only going to look at a few of the 100s of different kinds of cancer.
Of the 12 listed below, we’ll look at 6 of those in detail further below;
  1. Lung cancer – 1.56 million deaths annually, as of 2012
  2. Pancreatic cancer – 330,000 deaths globally
  3. Colorectal (colon) cancer – 610,000 deaths (Inflammatory bowel disease – 51,000 deaths in 2013 due to inflammatory bowel disease (largest influence to colorectal cancer) alone.)
  4. Breast cancer – 18.2% of all cancer deaths for men and women together or 283,920 deaths
  5. Liver cancer – In 2013, 300,000 deaths from liver cancer were due to hepatitis B, hepatitis C, or alcohol
  6. Thyroid cancer – in 2010, 36,000 deaths globally up from 24,000 in 1990.[35]Obesity may be associated with a higher incidence of thyroid cancer, but this relationship remains the subject of much debate.[36] 
  7. Ovarian cancer – estimated 15,000 deaths in 2008
  8. Cervical cancer – 266,000 deaths
  9. Prostate Cancer – In 2010 it resulted in 256,000 deaths up from 156,000 deaths in 1990.[155]
  10. Bladder cancer – is the 9th leading cause of cancer with 430,000 new cases[3]
  11. Kidney cancer –17,870 deaths in the US and the UK alone in 2012, with 208,000 new cases each year
  12. Endometrial cancer – caused 76,000 deaths
Let’s take a closer look at some of these types of cancer;
  • Lung cancer – 1.56 million deaths annually, as of 2012, is the most common cause of cancer in the US. The most common cause of lung cancer is smoking which warnings are required on cigarette packs.
  • Breast cancergallery-thumbnails– 18.2% of all cancer deaths for men and women together or 283,920 deaths is the second most common cause of cancer related deaths in women. Risk factors for developing breast cancer include: female sex, obesity, lack of physical exercise, drinking alcohol, hormone replacement therapy during menopauseionizing radiation, early age at first menstruation, having children late or not at all, older age, and family history.[2][4 There is a relationship between diet and breast cancer, including an increased risk with a high fat diet,[44] alcohol intake,[45] and obesity,[46] related to higher cholesterol levels.[47] In breast adipose tissue, overexpression of leptin leads to increased cell proliferation and cancer.[69] Dietary iodine deficiency may also play a role. [48] Don’t forget what increases leptin levels in the system more than anything else. What would happen to breast cancer if you removed wheat, sugar and grains from the diet? Would that decrease the expression leptin and put a hamper of the spread of cancer? A high fat diet, in this case would be a diet that creates a lot of fat. Carbs create fat. Eating fat doesn’t. I’ve never seen a warning about obesity and breast cancer, or that eating grain based foods can cause obesity. There should be.
  • Prostate Cancer – In 2010 it resulted in 256,000 deaths up from 156,000 deaths in 1990.[155]  is the leading cause of cancer death in males worldwide.   The data on the relationship between diet and prostate cancer is poor.[87] In light of this the rate of prostate cancer is linked to the consumption of the Western diet.[87] There is little if any evidence to support an association between trans fat, saturated fat and carbohydrate intake and risk of prostate cancer.[87][88] Evidence regarding the role of omega-3 fatty acids in preventing prostate cancer does not suggest that they reduce the risk of prostate cancer, although additional research is needed.[87][89] Vitamin supplements appear to have no effect and some may increase the risk.[9][87] High calcium intake has been linked to advanced prostate cancer.[90] Consuming fish may lower prostate cancer deaths but does not appear to affect its occurrence.[91] Some evidence supports lower rates of prostate cancer with a vegetarian diet.[92] There is some tentative evidence for foods containing lycopene and selenium.[93] Diets rich in cruciferous vegetables, soy, beans and other legumes may be associated with a lower risk of prostate cancer, especially more advanced cancers.[94]  Men who get regular exercise may have a slightly lower risk, especially vigorous activity and the risk of advanced prostate cancer.[94]
  • Colorectal cancer – 610,000 deaths (Inflammatory bowel disease – 51,000 deaths in 2013 due to inflammatory bowel disease (largest influence to colorectal cancer) alone.) IBD is a complex disease which arises as a result of the interaction of environmental and genetic factors. It is increasingly thought that alterations to enteral (probiotics?) bacteria can contribute to inflammatory gut diseases[20][21]IBD affected individuals have been found to have 30-50 percent reduced biodiversity of commensalism bacteria such as a decrease in Firmicutes (namely lachnosperacieae and Bacteroidetes), what I believe are pro-biotics (but I can’t find a definitive answer to that). Further evidence of the role of gut flora in the cause of inflammatory bowel disease is that IBD affected individuals are more likely to have been prescribed antibiotics in the 2-5 year period before their diagnosis than unaffected individuals.[22]The enteral bacteria can be altered by environmental factors, such as Concentrated milk fats (a common ingredient of processed foods and confectionery) or oral medications such as antibiotics and oral iron preparations.[23] This tells me that those who are taking headache medication (NSAIDs) often, are themselves open for colorectal cancer and one thing we know about wheat and grain consumption is that it causes headaches, forcing one to use NSAIDs for pain relief.
  • Liver cancer – In 2013, 300,000 deaths from liver cancer were due to hepatitis B, hepatitis C, or alcohol. Liver cancer, also known as hepatic cancer, is a cancer that originates in the liver. Liver tumors are discovered on medical imaging equipment (often by accident) or present themselves symptomatically as an abdominal mass, abdominal painyellow skin, nausea or liver dysfunction. The leading cause of liver cancer is cirrhosis due to either hepatitis B, hepatitis C, or alcohol.[1] Cirrhosis is most commonly caused by alcoholhepatitis Bhepatitis C, and non-alcoholic fatty liver disease.[1][2] Non-alcoholic fatty liver disease(NAFLD) is one of the causes of fatty liver, occurring when fat is deposited (steatosis) in the liver due to causes other than excessive alcohol use. NAFLD is related to insulin resistance and the metabolic syndrome and may respond to treatments originally developed for other insulin-resistant states (e.g.diabetes mellitus type 2) such as weight loss, metformin, and thiazolidinediones.[4] We know that carbohydrate consumption in the form of wheat and grains cause insulin resistance. Doesn’t it make sense then, that the consumption of wheat and grains has a major influence in liver cancer?
  • Kidney cancer – Factors that increase the risk of kidney cancer include smoking, which can double the risk of the disease; regular use of NSAIDs such as ibuprofen and naproxen, which may increase the risk by 51%[9] or may not;[10] obesity; faulty genes; a family history of kidney cancer; having kidney disease that needs dialysis; being infected with hepatitis C; and previous treatment for testicular cancer or cervical cancer. There are also other possible risk factors such as kidney stones [11] and high blood pressure, which are being investigated.[12] 17,870 deaths in the US and the UK alone in 2012, with 208,000 new cases each year
  • Bladder cancer – is the 9th leading cause of cancer with 430,000 new cases[3] and 165,000 deaths occurring in 2012.[4]  Urothelial carcinoma is a prototypical example of a malignancy arising from environmental carcinogenic influences. By far the important cause is cigarette smoking, which contributes to approximately half of the disease burden. Chemical exposures such as those sustained by workers in the petroleum industry, the manufacture of paints and pigments (prototypically aniline dyes), and agrochemicals are known to predispose to urothelial cancer. Interestingly, risk is lowered by increased liquid consumption, presumably as a consequence of increased urine production and thus less “dwell time” on the urothelial surface. Conversely, risk is increased among long-haul truck drivers and others in whom long urine dwell-times are encountered. As with most epithelial cancers, physical irritation has been associated with increased risk of malignant transformation of the urothelium. Thus, urothelial carcinomas are more common in the context of chronic urinary stone disease, chronic catheterization (as in patients with paraplegia or multiple sclerosis), and chronic infections. Some particular examples are listed below:

The one factor that intrigues me the most is the influence of agrochemicals, in the disease. Some of the most treated foods in our diet are wheat, corn, soy and grain based foods. They genetically modify these foods to withstand the rigors of agrochemicals like herbicides and insecticides, both of which contribute to bladder cancer. What is the one food that we were all told to eat the most of? Grains. If this one food were taken out of the diet, would that affect the numbers of people dying from bladder cancer? I think so. (I’m sure Monsanto doesn’t think so.)

Risk factors for pancreatic adenocarcinoma include:[2][3][4][32]

  1. Age, gender, and race; the risk of developing pancreatic cancer increases with age. Most cases occur after age 65,[4] while cases before age 40 are uncommon. The disease is slightly more common in men than women, and in the United States is over 1.5 times more common in African Americans, though incidence in Africa is low.[4]
  2. Cigarette smoking is the best-established avoidable risk factor for pancreatic cancer, approximately doubling risk among long-term smokers, the risk increasing with the number of cigarettes smoked and the years of smoking. The risk declines slowly after smoking cessation, taking some 20 years to return to almost that of non-smokers.[33]
  3. Obesity; a BMI greater than 35 increases relative risk by about half.[3]
  4. Family history; 5–10% of pancreatic cancer cases have an inherited component, where people have a family history of pancreatic cancer.[2] The risk escalates greatly if more than one first-degree relative had the disease, and more modestly if they developed it before the age of 50.[6] Most of the genes involved have not been identified.[2][34] Hereditary pancreatitis gives a greatly increased lifetime risk of pancreatic cancer of 30–40% to the age of 70.[5] Screening for early pancreatic cancer may be offered to individuals with hereditary pancreatitis on a research basis.[35] Some people may choose to have their pancreas surgically removed to prevent cancer developing in the future.[5]
    1. Pancreatic cancer has been associated with the following other rare hereditary syndromes: Peutz–Jeghers syndrome due to mutations in the STK11 tumor suppressor gene (very rare, but a very strong risk factor); dysplastic nevus syndrome (or familial atypical multiple mole and melanoma syndrome, FAMMM-PC) due to mutations in the CDKN2A tumor suppressor gene; autosomal recessiveataxia-telangiectasia and autosomal dominantly inherited mutations in the BRCA2gene and PALB2 gene; hereditary non-polyposis colon cancer (Lynch syndrome); and familial adenomatous polyposis. Pan NETs have been associated with multiple endocrine neoplasia type 1 (MEN1) and von Hippel Lindau syndromes.[2][5][6]
  5. Chronic pancreatitis appears to almost triple risk, and as with diabetes, new-onset pancreatitis may be a symptom of a tumor.[5] The risk of pancreatic cancer in individuals with familial pancreatitis is particularly high.[5][34]
  6. Diabetes mellitus is a risk factor for pancreatic cancer and (as noted in the Signs and symptoms section) new-onset diabetes may also be an early sign of the disease. People who have been diagnosed with Type 2 diabetes for longer than ten years may have a 50% increased risk, as compared with non-diabetics.[5]
  7. Specific types of food (as distinct from obesity) have not been clearly shown to increase the risk of pancreatic cancer.[2] Dietary factors for which there is some evidence of slightly increased risk include processed meatred meat, and meat cooked at very high temperatures (e.g. by frying, broiling or barbecuing).[36][37]

Highlighted areas are all wheat and grain caused conditions that would not exist if this food weren’t in our diet.

If 90 – 95% of all cases of cancer are due to lifestyle and behavioral factors, what does that say about our eating habits? Our eating habits are the most influential factor in anyone’s lifestyle. The old adage, “you are what you eat”, is more valid here, than anywhere else.

Our individual diets are what separate us from each other more than almost anything else, as that’s what distinguishes us from each other. In every diet, there exists one common thread throughout the world, and that’s grains, wheat in the western hemisphere and rice in the eastern hemisphere. They’re in every diet of every ethnicity. This is the one common thread that affects everyone on the planet. It does so simply because it’s in every diet on the planet, in some fashion or another.

As evidenced above, there are 6 types of cancer on this page, alone, in which wheat and grains play a part. If you eat food that causes cancer and you’ll more than likely, contract cancer.

What if this one factor was removed from the equation of cancer? What if wheat and grains were removed from our diets? What would happen if you took out that one factor in the equation of cancer, out of the equation? Would you still come still come up with the same result?

I contend that it would change the whole equation enough that the end result of cancer would inevitably be changed. This begs the question, if we removed wheat and grains from the diet, would that be a start for a cure for cancer?

I understand why a warning label is on every pack of cigarettes, one should be, we know that smoking causes lung cancer. If they put out warnings for something that may cause cancer, like processed meats and ‘fast foods’, why can’t they put out a warning for something that clearly causes cancer, sugar and wheat based products?

Hopefully, the day will come soon.

Next, we’ll take a closer look at cardiovascular diseases and grains influence there.

A thousand thanks to Wikipedia, I would have never been able to compile this without their help. 85% of this page came directly from Wkikpedia.