Elevated blood sugar is associated with colorectal cancer in postmenopausal women

Posted on December 3, 2011 by Dr. Jonathan

Summary: women in the highest third of blood glucose levels were almost twice as likely to develop colorectal cancer over the course of the study.

More evidence that high blood sugar contributes to cancer is presented in a study just published in the British Journal of Cancer that examines the link between elevated fasting glucose and colorectal cancer in postmenopausal women. The authors state:

“It is unclear whether circulating insulin or glucose levels are associated with increased risk of colorectal cancer. Few prospective studies have examined this question, and only one study had repeated measurements.”

So they examined baseline fasting serum insulin and glucose values for 4902 non-diabetic women over 12 years, during which 81 cases of colorectal cancer turned up. The data showed a significant trend:

“Baseline glucose levels were positively associated with colorectal cancer and colon cancer risk: multivariable-adjusted hazard ratio (HR) comparing the highest (greater than or equal to 99.5 mg dl−1) with the lowest tertile (<89.5 mg dl−1): 1.74 and 2.25, respectively. Serum insulin and homeostasis model assessment were not associated with risk.”

In other words, glucose in the highest third almost doubles the risk. In this non-diabetic group an association with fasting insulin levels was not observed. However, I can say through extensive experience over 2-3 years having patients suffer through an extended glucose + insulin tolerance test that insulin can be often elevated later in the test but not in the fasting sample. The authors conclude:

“These data suggest that elevated serum glucose levels may be a risk factor for colorectal cancer in postmenopausal women.”

Elevated fasting blood sugar is a risk factor for prostate enlargement

Posted on November 26, 2011 by Dr. Jonathan

Summary: in this study prostate size correlated with fasting blood sugar. Elevated fasting glucose is a risk factor for prostate disease.

A study recently published in the Journal of Korean Medical Science offers further evidence for the association between blood glucose regulation and prostate disease. The authors state:

“We evaluated the correlations between BMI, fasting glucose, insulin, testosterone level, insulin resistance, and prostate size in non-diabetic benign prostatic hyperplasia (BPH) patients with normal testosterone levels.”

They examined ata from 212 non-diabetic BPH patients with normal testosterone levels, excluding those with diabetes or serum testosterone levels less than 3.50 ng/mL. Their data showed that…

“Prostate size correlated positively with age, PSA , and fasting glucose level, but not with BMI, testosterone, insulin level, or HOMA-IR.Testosterone level inversely correlated with BMI, insulin level, and HOMA-IR [insulin resistance], but not with age, prostate size, PSA, or fasting glucose. HOMA-IR significantly correlated with BMI, fasting glucose, and insulin level, but not with age, PSA, or prostate size.”

There seems to be a disconnect here regarding the association of prostate size with fasting glucose but not the calculated insulin resistance that requires further investigation. The authors, however, are clear in their conclusion regarding blood sugar and prostate hypertrophy:

“In non-DM BPH patients with normal testosterone levels, fasting glucose level is an independent risk factor for prostate hyperplasia.”

Most US doctors are still not paying proper attention to blood sugar

Posted on October 30, 2010 by Dr. Jonathan

It’s disturbing and worrisome to see how few doctors seem to be alert to the blood sugar dysregulation that precedes type 2 diabetes and many other chronic diseases in their patients as evidenced by a study just published in the journal Diabetes Care. The authors conducted their investigation to…

“…estimate the rates of prevalence, diagnosis, and treatment of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT).”

They examined a representative sample of the U.S. population that included 1,547 nondiabetic adults without a history of heart attack to determine the proportion who met the criteria for IFG/IGT, and the proportion of them who: 1) received a diagnosis from their physicians; 2) were prescribed lifestyle modification or medication for blood sugar; or 3) were currently on therapy. Their data painted a dismal picture:

“Of the 1,547 subjects, 34.6% had pre-diabetes; 19.4% had IFG only; 5.4% had IGT only, and 9.8% had both IFG and IGT. Only 4.8% of those with pre-diabetes reported having received a formal diagnosis from their physicians. No subjects with pre-diabetes received oral antihyperglycemics, and the rates of recommendation for exercise or diet were 31.7% and 33.5%, respectively.”

Yikes. It’s really up to the patient to be informed (one of the purposes of this blog) and seek proper care. Blood sugar dysregulation wrecks almost everything that clinicians practicing according to the functional model try to do to correct brain, hormone and immune dysregulation. It’s importance as a clinical focus is hard to over-emphasize. The authors’ disappointment is almost palpable in their conclusion:

“Three years after a major clinical trial demonstrated that interventions could greatly reduce progression from IFG/IGT to type 2 diabetes, the majority of the U.S. population with IFG/IGT was undiagnosed and untreated with interventions. Whether this is due to physicians being unaware of the evidence, unconvinced by the evidence, or clinical inertia is unclear.”

Perhaps this says something about why the scientists who authored another paper in the same issue of Diabetes Care saw fit to ask whether sugar-sweetened beverages would contribute to the risk of metabolic syndrome and type 2 diabetes (!):

“Consumption of sugar-sweetened beverages (SSBs), which include soft drinks, fruit drinks, iced tea, and energy and vitamin water drinks has risen across the globe. Regular consumption of SSBs has been associated with weight gain and risk of overweight and obesity, but the role of SSBs in the development of related chronic metabolic diseases, such as metabolic syndrome and type 2 diabetes, has not been quantitatively reviewed.”

Their meta-analysis included 310,819 participants from 11 acceptable studies. It’s troubling to allow that there may be physicians who might not anticipate the conclusion that their data defined:

“In addition to weight gain, higher consumption of SSBs is associated with development of metabolic syndrome and type 2 diabetes. These data provide empirical evidence that intake of SSBs should be limited to reduce obesity-related risk of chronic metabolic diseases.”

It seems that even fewer physicians and their patients are aware of the role of glucose in ‘feeding’ cancer and the research being done to block the metabolism of sugar by tumor cells as described in a paper just published in the journal Oncogene. The authors state:

“Tumors show an increased rate of glucose uptake and utilization. For this reason, glucose analogs are used to visualize tumors by the positron emission tomography technique, and inhibitors of glycolytic metabolism are being tested in clinical trials.”

While research investigates possible interventions to aggressively interrupt the glycolytic metabolism of tumor cells, doctors should assist their patients in controlling blood sugar and insulin (another tumor promoter) with the appropriate tools:

“Upregulation of glycolysis confers several advantages to tumor cells: it promotes tumor growth and has also been shown to interfere with cell death at multiple levels…Moreover, inhibition of glucose metabolism sensitizes cells to death ligands. Glucose deprivation and antiglycolytic drugs induce tumor cell death…”

Blood sugar dysregulation contributes to most chronic diseases including cardiovascular, autoimmune, neurodegenerative and malignant conditions. Supporting healthy blood sugar and insulin regulation is one of the most important things that practitioners and their patients can do together.

Elevated blood sugar increases risk of cancer

Posted on September 9, 2010 by Dr. Jonathan

A research article just published in PLoS (Public Library of Science) Medicine adds more evidence to the association between elevated blood sugar and cancer. The authors begin by stating:

“Prospective studies have indicated that elevated blood glucose levels may be linked with increased cancer risk…The aim of this study was to investigate the association between blood glucose and risk of incident and fatal cancer overall and at specific sites, as well as all-cause mortality, in a large study of six European cohorts including correction for random error in glucose levels..”

The Metabolic Syndrome and Cancer project (Me-Can) includes 274,126 men and 275,818 women from Norway, Austria and Sweden whose average age at the beginning of observation was 44.8 years. Over an average follow-up time of 10.4 years 18,621 men and 11,664 women were diagnosed with cancer, and 6,973 men and 3,088 women died of cancer. When the authors calculated the relative risk for glucose levels (adjusting for BMI and smoking), the data made a strong statement:

“Significant increases in risk among men were found for incident and fatal cancer of the liver, gallbladder, and respiratory tract, for incident thyroid cancer and multiple myeloma, and for fatal rectal cancer. In women, significant associations were found for incident and fatal cancer of the pancreas, for incident urinary bladder cancer, and for fatal cancer of the uterine corpus, cervix uteri, and stomach.”

The authors discuss the possible mechanisms:

“Insulin and bioavailable insulin-like growth factor-I (IGF-I) are possible links between glucose and cancer; hyperglycaemia induces elevation of these hormones that stimulate tumour growth. Glucose may also have a direct tumour-promoting effect as glucose is used as an energy substrate in tumour cells, particularly in fast-growing, highly proliferative tumour cells.”

They boil down their findings in this closing summary:

“In conclusion, abnormal glucose metabolism, independent of BMI, is associated with increases in risk of cancer and cancer death overall and at many specific sites. Furthermore, our data showed a linear and somewhat stronger association among women than among men, and the association was stronger for fatal compared to incident cancer.”

Blood sugar and the brain in learning and behavioral disorders

Posted on September 5, 2010 by Dr. Jonathan

The brain needs a steady supply of glucose to work normally. Disorders of blood sugar regulation, whether hypoglycemia or insulin resistance (precursor to type 2 diabetes), deprives the brains cells of the fuel to produce the energy they need to function. Research just published in the journal Diabetologia examines the cognitive impairments present in adolescents when insulin resistance and overweight have progressed to type 2 diabetes.

“Central nervous system abnormalities, including cognitive and brain impairments, have been documented in adults with type 2 diabetes…Assessing adolescents with type 2 diabetes will allow the evaluation of whether diabetes per se may adversely affect brain function and structure years before clinically significant vascular disease develops.”

The authors compared two groups of overweight adolescents, one with and the other without type 2 diabetes. The depredations of insulin resistance on the brain were stunning:

“Adolescents with type 2 diabetes performed consistently worse in all cognitive domains assessed, with the difference reaching statistical significance for estimated intellectual functioning, verbal memory and psychomotor efficiency…[and] executive function, reading and spelling. MRI-based automated brain structural analyses revealed both reduced white matter volume and enlarged cerebrospinal fluid space in the whole brain and the frontal lobe in particular… In addition, assessments using diffusion tensor imaging revealed reduced white and grey matter microstructural integrity.”

The authors conclusion places both clinicians and parents on the alert:

“These abnormalities are not likely to result from education or socioeconomic bias and may result from a combination of subtle vascular changes, glucose and lipid metabolism abnormalities and subtle differences in adiposity in the absence of clinically significant vascular disease.”

On the hypoglycemic pole of glucose regulation we can appreciate earlier fascinating research published Pediatric Research documenting an impaired neurotransmitter response to falling blood sugar in children with ADD (the catecholamines epinephrine and norepinephrine attenuate the drop in blood sugar).

“Eating simple sugars has been suggested as having adverse behavioral and cognitive effects in children with attention deficit disorder (ADD)…metabolic, hormonal, and cognitive responses to a standard oral glucose load (1.75 g/kg) were compared in 17 children with ADD and 11 control children.”

Their data showed a significant difference between ADD and control children:

“The late glucose fall stimulated a rise in plasma epinephrine that was nearly 50% lower in ADD than in control children. Plasma norepinephrine levels were also lower in ADD than in control children…”

The authors’ conclusion indicates the need for conscientious blood sugar management through dietary and other measures:

“These data suggest that children with ADD have a general impairment of sympathetic activation involving adrenomedullary as well as well as central catecholamine regulation [of blood sugar].”

Similar phenomena are presented in a paper published in the Journal of the American Academy of Child & Adolescent Psychiatry describing abnormalities of brain metabolism in girls with ADHD:

“This study assesses the effect of attention-deficit hyperactivity disorder (ADHD) and gender on cerebral glucose metabolism (CMRglu), using positron emission tomography and 18F-fluorodeoxyglucose.”

An interesting gender difference emerged from the data:

“However, the global CMRglu in ADHD girls was 15.0% lower than in normal girls, while global CMRglu in ADHD boys was not different than in normal boys. Furthermore, global CMRglu in ADHD girls was 19.6% lower than in ADHD boys and was not different between normal girls and normal boys.”

Gender differences that must be respected are pronounced here and throughout medicine and biology:

“The greater brain metabolism abnormalities in females than males strongly stress that more attention be given to the study of girls with ADHD.”

Addressing the dysfunctions in blood sugar dysregulation associated with disorders of learning and behavior requires understanding that deleterious eating conducts can manifest as a form of self-medication. A paper recently published in Current Psychiatry Reports brings attention to this:

“In the past decade, we have become increasingly aware of strong associations between overweight/obesity and symptoms of attention-deficit/hyperactivity disorder (ADHD) in children, adolescents, and adults.”

The need to satisfy imperious physiological urges on a cellular level when an individuals genetic needs are not being met can overwhelm all advice and intention to acquire more wholesome and sustainable habits:

“It is also proposed—based on the compelling evidence that foods high in fat, sugar, and salt are as addictive as some drugs of abuse—that excessive food consumption could be a form of self-medication. This view conforms with the well-established evidence that drug use and abuse are substantially higher among those with ADHD than among the general population.”

True remediation demands a functional medicine approach to resolve the underlying cellular and metabolic needs that are not being met so they can be supported in a physiological and sustainable manner to restore normal function.

A paper published in the Journal of Nutrition, Health & Aging brings us back to the fundamental importance of glucose regulation for the brain.

“The regulation of glycaemia (thanks to the ingestion of food with a low glycaemic index ensuring a low insulin level) improves the quality and duration of intellectual performance, if only because at rest the brain consumes more than 50% of dietary carbohydrates, approximately 80% of which are used only for energy purpose. In infants, adults and aged, as well as in diabetes, poorer glycaemic control is associated with lower performances, for instance on tests of memory. At all ages, and more specifically in aged people, some cognitive functions appear sensitive to short term variations in glucose availability.“

Cancer cells have a ‘sweet tooth’ for fructose too

Posted on August 7, 2010 by Dr. Jonathan

It’s long been known that cancer cells have a ‘sweet tooth’—relying mainly on aerobic glycolysis for their energy needs, and that increased refined carbohydrate consumption feeds cancer growth (the Warburg effect). This phenomenon has been investigated mostly in relation to glucose. A study just published in the journal Cancer Research provides evidence that fructose has a similar effect. The authors observe:

“Carbohydrate metabolism via glycolysis and the tricarboxylic acid cycle is pivotal for cancer growth, and increased refined carbohydrate consumption adversely affects cancer survival.”

Noting that fructose consumption has increased dramatically and that glucose and fructose are transported and metabolized differently, they investigated whether fructose could fuel the growth of cancer cells similar to the way glucose does. Their findings are of great importance to both patients and clinicians:

“Here, we report that fructose provides an alternative substrate to induce pancreatic cancer cell proliferation…These findings show that cancer cells can readily metabolize fructose to increase proliferation.”

The significance of diet and metabolic support for individuals with cancer is hard to overstate:

“They [these findings] have major significance for cancer patients given dietary refined fructose consumption, and indicate that efforts to reduce refined fructose intake or inhibit fructose-mediated actions may disrupt cancer growth.”

Kidney damage can occur before diabetes sets in

Posted on April 26, 2010 by Dr. Jonathan

Clinical Journal of the Amer Soc of Nephro An important study just published in the Clinical Journal of the American Society of Nephrology that offers powerful evidence for the need to maintain healthy insulin and glucose levels well before that system fails and blood sugar crosses the line into the type 2 diabetes territory. High levels of insulin do nasty mischief throughout the body and the kidneys are especially sensitive. The authors set out with this objective:

“Prevalence of chronic kidney disease (CKD) in people with diagnosed diabetes is known to be high, but little is known about the prevalence of CKD in those with undiagnosed diabetes or prediabetes. We aimed to estimate and compare the community prevalence of CKD among people with diagnosed diabetes, undiagnosed diabetes, prediabetes, or no diabetes.”

Their data paints a worrisome picture:

“Fully 39.6% of people with diagnosed and 41.7% with undiagnosed diabetes had CKD…Among those with CKD, 39.1% had undiagnosed or prediabetes.”

Remember dear reader that chronic kidney disease means that there has been an irretrievable loss of kidney tissue; this is beyond normal age-related changes. This is yet another important reason to confirm that your strategy for maintaining healthy insulin function is suiting your needs. This is not difficult to determine with the right test assessment. The authors conclude:

“CKD prevalence is high among people with undiagnosed diabetes and prediabetes. These individuals might benefit from interventions aimed at preventing development and/or progression of both CKD and diabetes.”

Fructose even worse than glucose for fat and insulin

Posted on January 12, 2010 by Dr. Jonathan

This is why the ubiquitous high-fructose corn syrup is such a disaster for public health. The authors of this study published in The Journal of Clinical Investigation note that “Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance.” When they examined the effect in humans they found that all the following were increased markedly in the subjects on fructose but not glucose: visceral adiposity (fat around the organs), plasma triglycerides, fat in the liver, small dense LDL, oxidized LDL, fasting glucose and fasting insulin. At the same time insulin sensitivity decreased in the subjects consuming fructose but not glucose. The authors conclude: “These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.” [DNL = de novo lipogenesis which means making fat from scratch in the liver.] An accompanying commentary in the same journal states: “In the event that any readers harbor some remaining skepticism, an unprecedented thorough analysis in close to 900,000 participants from almost 60 prospective studies was very recently published, proving beyond any possible doubt that progressive excess mortality is caused by increased body adiposity…Stanhope and colleagues provide major scientific progress by demonstrating marked differences in the metabolic effects of these two major sugars with respect to their ability to promote intraabdominal lipid deposition and hepatic lipid production, while shifting cholesterol metabolism in an unfavorable manner and diminishing insulin sensitivity in humans.” Public health is groaning under a burden of overweight/obesity; how much disease could we prevent just by cutting out most of the sweet drinks (including most fruit juices) for children and adults?

Sugar shortens life span

Posted on November 25, 2009 by Dr. Jonathan

You are probably aware of earlier studies that demonstrated increase in life span of experimental animals by the effect of caloric restriction on insulin regulating pathways. This interesting study recently published in the journal Cell Metabolism elucidates the flip side: “We found that adding a small amount of glucose to the medium (2%) shortened the life span of C. elegans by inhibiting the activities of life span-extending transcription factors that are also inhibited by insulin signaling…” The authors conclude: “Together, these findings raise the possibility that a low-sugar diet might have beneficial effects on life span in higher organisms.”