Worm Menu, War Menu or Worm in You?

You have heard it said, “You are what you eat.” Well I believe it better said, “You eat what you are fed by those you are feeding, and then you eat them.”

Feces, also spelled faeces, also called excrement, solid bodily waste discharged from the large intestine through the anus during defecation. Feces are normally removed from the body one or two times a day. About 100 to 250 grams (3 to 8 ounces) of feces are excreted by a human adult daily.

Normally, feces are made up of 75 percent water and 25 percent solid matter. About 30 percent of the solid matter consists of dead bacteria; about 30 percent consists of indigestible food matter such as cellulose; 10 to 20 percent is cholesterol and other fats; 10 to 20 percent is inorganic substances such as calcium phosphate and iron phosphate; and 2 to 3 percent is protein.

Cell debris shed from the mucous membrane of the intestinal tract also passes in the waste material, as do bile pigments (bilirubin) and dead leukocytes (white blood cells). The brown colour of feces is due to the action of bacteria on bilirubin, which is the end product of the breakdown of hemoglobin (red blood cells). The odour of feces is caused by the chemicals indole, skatole, hydrogen sulfide, and mercaptans, which are produced by bacterial action.

Many diseases and disorders can affect bowel function and produce abnormalities in the feces. Constipation is characterized by infrequent evacuations and the production of excessively hard and dry feces, while diarrhea results in frequent defecation and excessively soft, watery feces. Bleeding in the stomach or intestines may result in the passage of blood with the stool, which appears dark red, tarry, or black. Fatty or greasy stools usually indicate pancreatic or small-intestine afflictionsTyphoidcholera, and amoebic dysentery are among diseases spread by the contamination of food with the feces of infected persons.

More on Vitamin D, Ergosterol and Cholesterol

Do Vitamin D Levels Affect Cholesterol?

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Higher vitamin D levels appear to be associated with higher total cholesterol levels and higher HDL cholesterol levels, according to a new study presented at the American College of Cardiology’s (ACC) 65th Annual Scientific Sessions.1 

Investigators looked 13 039 adults and found that higher 25-hydroxyvitamin D (25[OH]D) was cross-sectionally and prospectively associated with higher total cholesterol and HDL cholesterol levels and lower total cholesterol-to-HDL cholesterol ratio after considering factors such as diabetes and adiposity.

“We wanted to see the association of low vitamin D with low HDL cholesterol and high total cholesterol-to-HDL cholesterol ratio, but I think we were most surprised to not find an association of vitamin D deficiency with elevated triglycerides, as has been noted in other studies. This may be in part that we carefully adjusted for other confounding lifestyle variables such as physical activity and 2 measures of adiposity (BMI and waist circumference),” said senior study author Erin Michos, MD, MHS, associate professor of medicine and epidemiology and associate director of preventive cardiology at Johns Hopkins School of Medicine in Baltimore.

“We also were surprised that we did not see any association of low vitamin D with elevated LDL cholesterol in our overall sample. However, when we performed a sensitivity analysis looking at individuals who were not taking lipid-lowering therapy at the baseline exam or at any of the follow-up visits, we did see the association of low vitamin D with elevated LDL cholesterol.”

Dr Michos and her colleagues measured lipids at baseline (1990-1992), in 1993-1994, and in 1996-1998. The mean follow-up was 5.2 years.

The investigators used linear and mixed model regression methods to assess associations of 25(OH) D with cross-sectional and lipid trends. They also adjusted for clinical characteristics. The mean age at baseline was 57.6 years, 57% were women, and 24% were black.

Among those individuals without baseline dyslipidemia, participants with low 25(OH) D (<20 ng/mL) compared with optimal levels (≥30 ng/mL) had increased risk for incident dyslipidemia in demographic-adjusted models (hazard ratio [HR]=1.19; 95% CI, 1.02-1.39). Nevertheless, this finding was attenuated in fully-adjusted models (HR=1.12; 95% CI, 0.95-1.32).1

Dr Michos said low concentrations of vitamin D, defined as serum 25(OH)D below 30 ng/mL, are present in more than two-thirds of the US adult population and in an estimated 1 billion individuals worldwide. 

“So, this is a major relevant public health issue. Vitamin D deficiency has been associated with a number of non-bone-related adverse health outcomes, including increased risk for cardiovascular diseases (CVDs). One of the mechanisms by which vitamin D may influence CVD risk is through an effect on lipids,” Dr Michos told Endocrinology Advisor. “The potential link between vitamin D deficiency and adverse lipid profile should be of great interest to a large number of practitioners who treat both vitamin D and lipid disorders, including endocrinologists, internists, lipidologists, and cardiologists.”

Previous studies, including one study conducted by her team and recently published in the Journal of Clinical Lipidology, suggested that low levels of vitamin D were associated with an atherogenic lipid profile consisting of elevated LDL cholesterol, elevated triglycerides, and lower HDL cholesterol, noted Dr Michos.2 However, most of the evidence supporting this association was obtained in cross-sectional analyses. 

For this current investigation, the researchers analyzed the association between vitamin D status and the lipid profile prospectively using data from the Atherosclerosis Risk in Communities (ARIC) study. This large study of a US community-based sample of blacks and whites collected data on numerous demographic, lifestyle, and clinical variables spanning multiple clinic visits. Unlike prior investigations, ARIC allowed for extensive adjustment of possible confounders over time, according to Dr Michos. It also contained information regarding initiation of lipid-lowering medication use during follow-up. 

Dr Michos said further research is warranted, including randomized, controlled trials, to assess whether treating vitamin D deficiency can impact lipids and thereby influence CVD risk.

References

  1. Faridi K, Zhao D, Martin SS, et al. Vitamin D and Change in Lipids Over 5 Years: The Atherosclerosis Risk in Communities (ARIC) Study. Presented at: ACC 65th Annual Scientific Session & Expo; April 2-4, 2016; Chicago, IL.
  2. Lupton JR, Faridi KF, Martin SS, et al. Deficient serum 25-hydroxyvitamin D is associated with an atherogenic lipid profile: The Very Large Database of Lipids (VLDL-3) study. J Clin Lipidol. 2016;10(1):72-81. doi:10.1016/j.jacl.2015.09.006.

Statin Therapy and Decreased Incidence of Positive Candida Cultures Among Patients With Type 2 Diabetes Mellitus Undergoing Gastrointestinal Surgery

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OBJECTIVE

To assess whether statin therapy decreases the incidence of cultures positive for Candida species among high-risk hospitalized patients with type 2 diabetes mellitus (DM).

PATIENTS AND METHODS

We performed a retrospective cohort study analyzing the records of all patients with type 2 DM who were admitted to Massachusetts General Hospital for lower gastrointestinal tract surgery between January 1, 2001, and May 1, 2008. We defined statin exposure as the filling of at least 1 prescription of statins during the 6 months before hospitalization or during the current hospital stay. The primary outcome was a culture positive for Candida species during hospitalization. Clinical information on a wide range of covariates was collected. Logistic regression analysis was used to adjust for possible confounders.

RESULTS

Of the 1019 patients who were eligible for the study, 493 (48%) were receiving statins. A total of 139 patients (14%) had at least 1 culture positive for Candida species during hospitalization. An adjusted multivariate model based on a backward stepwise elimination procedure showed that statin therapy significantly decreased the incidence of cultures positive for Candida species (odds ratio, 0.60; 95% confidence interval [CI], 0.38-0.96; P=.03) with a statistically significant prolonged time to event compared with no statin therapy (adjusted hazard ratio, 0.62; 95% CI, 0.44-0.88; P=.01). The benefit of statins was more prominent in patients with type 2 DM who had greater comorbidities (Charlson Comorbidity Index ≥2) (adjusted odds ratio, 0.47; 95% CI, 0.27-0.79; P=.01).

CONCLUSION

Among patients with type 2 DM who underwent gastrointestinal surgery, use of statins correlated with a decreased incidence of cultures positive for Candida species.

Biological consequences of statins in Candida species and possible implications for human health

Content Source – National Institutes for Health

The statins, simvastatin and atorvastatin are the most widely prescribed drugs. Statins lower cholesterol levels through their action on HMG-CoA (3-hydroxy-3-methylglutaryl-CoA) reductase, an essential enzyme for the biosynthesis of cholesterol. Fungal HMG-CoA reductases are also inhibited by statins, resulting in reduced levels of ergosterol (the fungal equivalent of cholesterol) and concomitant growth inhibition. This effect occurs in a range of fungal species and possibly affects fungal colonization of people on statin therapy. Furthermore, it may suggest that statins could have a role in new antifungal therapies. Possibly associated with the reduction in ergosterol levels, statins also inhibit respiratory growth. In the yeast, Candida glabrata, passage with statins dramatically increased the frequencies of petite mutants that were devoid of mitochondrial DNA, suggesting that statins caused a defect in the maintenance of mitochondrial DNA. These observations in C. glabrata may provide further insights into side effects of statins in humans undergoing treatment for hypercholesterolaemia. In addition, C. glabrata may be highly useful for the preliminary screening of agents to reduce statin side effects.

Antifungal activity of statins against Aspergillus species

Content Source – National Institutes for Health

The cholesterol-lowering agents known as statins have in vitro activities against human pathogenic fungi, such as Candida species, Cryptococcus neoformans, and Zygomycetes. Synergy between statins and azoles against these fungi has also been reported. We evaluated the in vitro activities of two statins, lovastatin and simvastatin, alone and in combination with azoles and amphotericin B, against clinical isolates of Aspergillus spp. A disk diffusion assay showed that both statins were active against Aspergillus spp. The minimal inhibitory concentration (MIC) ranges for lovastatin and simvastatin against Aspergillus spp. were 16 to >256 microg/ml and 4 to >256 microg/ml, respectively. Although both statins were fungicidal for A. fumigatus, the MICs were vastly higher than clinically achievable concentrations. The results of a combined agar dilution-Epsilometer test as well as a disk diffusion assay showed that neither statin had any effect on the in vitro activities of itraconazole, voriconazole, or amphotericin B against Aspergillus spp.