Awareness of social care needs in people with epilepsy and intellectual disability.

BACKGROUND: Nearly a quarter of people with intellectual disability (ID) have epilepsy with large numbers experiencing drug-resistant epilepsy, and premature mortality. To mitigate epilepsy risks the environment and social care needs, particularly in professional care settings, need to be met. PURPOSE: To compare professional care groups as regards their subjective confidence and perceived responsibility when managing the need of people with ID and epilepsy. METHOD: A multi-agency expert panel developed a questionnaire with embedded case vignettes with quantitative and qualitative elements to understand training and confidence in the health and social determinants of people with ID and epilepsy. The cross-sectional survey was disseminated amongst health and social care professionals working with people with ID in the UK using an exponential non-discriminative snow-balling methodology. Group comparisons were undertaken using suitable statistical tests including Fisher's exact, Kruskal-Wallis, and Mann-Whitney. Bonferroni correction was applied to significant (p < 0.05) results. Content analysis was conducted and relevant categories and themes were identified. RESULTS: Social and health professionals (n = 54) rated their confidence to manage the needs of people with ID and epilepsy equally. Health professionals showed better awareness (p < 0.001) of the findings/recommendations of the latest evidence on premature deaths and identifying and managing epilepsy-related risks, including the relevance of nocturnal monitoring. The content analysis highlighted the need for clearer roles, improved care pathways, better epilepsy-specific knowledge, increased resources, and better multi-disciplinary work. CONCLUSIONS: A gap exists between health and social care professionals in awareness of epilepsy needs for people with ID, requiring essential training and national pathways.

DNA repair and response to sperm DNA damage in oocytes and embryos, and the potential consequences in ART: a systematic review.

Sperm DNA damage is considered a predictive factor for the clinical outcomes of patients undergoing ART. Laboratory evidence suggests that zygotes and developing embryos have adopted specific response and repair mechanisms to repair DNA damage of paternal origin. We have conducted a systematic review in accordance with guidelines from Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) to identify and review the maternal mechanisms used to respond and repair sperm DNA damage during early embryonic development, how these mechanisms operate and their potential clinical implications. The literature search was conducted in Ovid MEDLINE and Embase databases until May 2021. Out of 6297 articles initially identified, 36 studies were found to be relevant through cross referencing and were fully extracted. The collective evidence in human and animal models indicate that the early embryo has the capacity to repair DNA damage within sperm by activating maternally driven mechanisms throughout embryonic development. However, this capacity is limited and likely declines with age. The link between age and decreased DNA repair capacity could explain decreased oocyte quality in older women, poor reproductive outcomes in idiopathic cases and patients who present high sperm DNA damage. Ultimately, further understanding mechanisms underlying the maternal repair of sperm DNA damage could lead to the development of targeted therapies to decrease sperm DNA damage, improved oocyte quality to combat incoming DNA insults or lead to development of methodologies to identify individual spermatozoa without DNA damage.

Dealer's Dytonia (Croupier's Cramp) - An Unusual Hazard Of Gambling.

Dystonia takes many forms and often presents acutely to emergency care. The diagnosis is often delayed because it mimics other more common conditions. This report describes a patient with a rare occupational dystonia, the typical clinical features of dystonia in general, and differentials to consider.

Male patients affected by mosaic PCDH19 mutations: five new cases.

Pathogenic variants in the PCDH19 gene are associated with epilepsy, intellectual disability (ID) and behavioural disturbances. Only heterozygous females and mosaic males are affected, likely due to a disease mechanism named cellular interference. Until now, only four affected mosaic male patients have been described in literature. Here, we report five additional male patients, of which four are older than the oldest patient reported so far. All reported patients were selected for genetic testing because of developmental delay and/or epilepsy. Custom-targeted next generation sequencing gene panels for epilepsy genes were used. Clinical data were collected from medical records. All patients were mosaic in blood for likely pathogenic variants in the PCDH19 gene. In most, clinical features were very similar to the female phenotype, with normal development before seizure onset, which occurred between 5 and 10 months of age, clustering of seizures and sensitivity to fever. Four out of five patients had mild to severe ID and behavioural problems. We reaffirm the similarity between male and female PCDH19-related phenotypes, now also in a later phase of the disorder (ages 10-14 years).

Cardiovascular risk reduction in hypertension: angiotensin-converting enzyme inhibitors, angiotensin receptor blockers. Where are we up to?

Previously, management of hypertension has concentrated on lowering elevated blood pressure. However, the target has shifted to reducing absolute cardiovascular (CV) risk. It is estimated that two in three Australian adults have three or more CV risk factors at the same time. Moderate reductions in several risk factors can, therefore, be more effective than major reductions in one. When managing hypertension, therapy should be focused on medications with the strongest evidence for CV event reduction, substituting alternatives only when a primary choice is not appropriate. Hypertension management guidelines categorise angiotensin-converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) interchangeably as first-line treatments in uncomplicated hypertension. These medications have different mechanisms of action and quite different evidence bases. They are not interchangeable and their prescription should be based on clinical evidence. Despite this, currently ARB prescriptions are increasing at a higher rate than those for ACEI and other antihypertensive classes. Evidence that ACEI therapy prevents CV events and death, in patients with coronary artery disease or multiple CV risk factors, emerged from the European trial on reduction of cardiac events with perindopril in stable coronary artery disease (EUROPA) and Heart Outcomes Prevention Evaluation (HOPE) trials respectively. The consistent benefit has been demonstrated in meta-analyses. The clinical trial data for ARB are less consistent, particularly regarding CV outcomes and mortality benefit. The evidence supports the use of ACEI (Class 1a) compared with ARB despite current prescribing trends.

Periodontitis is associated with altered plasma fatty acids and cardiovascular risk markers.

BACKGROUND AND AIMS: In periodontitis it has been found that some perturbation exists in lipid biomarkers, such as increased serum total cholesterol and low-density lipoprotein cholesterol. Nevertheless, the relationship between fatty acids and periodontitis has been demonstrated only in a few studies and remains controversial. The aim of this investigation was to explore the effects of periodontitis on a cluster of traditional and novel cardiovascular risk factors such as plasma-lipids profile, types of plasma fatty acids, adhesion molecules and systemic inflammatory markers. METHODS AND RESULTS: At a university dental school, 56 patients all over 35 years old were enrolled and invited to participate in the study. Total plasma fatty acids, saturated, n-6 polyunsaturated and monounsaturated fatty acids, peroxidability index, soluble VCAM, TNF-alpha, cholesterol, triacylglycerols, and VLDL-c were significantly higher in the periodontitis group compared to the non-periodontitis group. CONCLUSIONS: This close association found between plasma triacylglycerols, LDL-c, saturated fatty acids, polyunsaturated fatty acids, total amount of fatty acids and coenzyme Q(10) with some periodontal data such as periodontal probing depth, recession of the gingival margin and clinical attachment level (Pearson correlation between 0.3 and 0.6), leads to the conclusion that there is an inter-relationship between periodontitis, plasma fatty acids profile and the increase in metabolic risk factors for cardiovascular diseases.

Nifedipine and cyclosporin affect fibroblast calcium and gingiva.

It has been stated that cyclosporin and nifedipine produce gingival overgrowth. However, the specific pathogenic mechanism remains uncertain. We used an experimental rat model to test the hypothesis that changes in collagen metabolism and numbers of gingival blood vessels are not mediated by intracellular calcium concentration (ratiometric Fura-2 AM measurement) in gingival fibroblasts. In the cyclosporin group, both width (364.2 +/- 67.5 mum) and microvessel density (number of vessels/mm(2), stained with anti-CD34 antibody) (41.6 +/- 5.1) of gingiva were statistically different when compared with those in the control group (width = 184.3 +/- 35.2 mum, microvessel density = 19.6 +/- 2.4). The nifedipine group showed the highest content of collagen (proportion of total stroma occupied by collagen, stained with Picro-Mallory) (nifedipine group = 66.3 +/- 9.4, cyclosporin group = 55.2 +/- 7.9, control group = 30.1 +/- 10.2). Freshly cultured fibroblasts from the cyclosporin group exhibited higher ratiometric values of fluorescence than did both the control and nifedipine groups (p = 0.03). Our results support the hypothesis that changes in gingival collagen metabolism are not mediated by calcium intracellular oscillations.

Inhibition of macrophage-mediated tumor cell destruction by oxidized lipoproteins.

Lipoproteins (LP), isolated from human sera by column chromatography and density ultracentrifugation, were tested for their ability to inhibit macrophage (M phi)-mediated tumor cell destruction. None of the LP subclasses isolated by ultracentrifugation inhibited M phi-mediated cytolysis. Chromatography on a Sephadex G-200 column, prior to or following ultracentrifugation, resulted in the isolation of very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) that prevented tumor cell destruction by M phi. High-density lipoprotein did not acquire the ability to inhibit M phi-mediated tumor cell killing under any condition. The acquisition of inhibitory activity by VLDL and LDL subclasses could be prevented by incorporation of EDTA and the bubbling of nitrogen gas into the chromatography buffer. These conditions inhibited the formation of lipid peroxides and thus prevented the formation of LP that inhibit M phi-mediated cytotoxicity. The mechanism by which oxidized LP prevents M phi from destroying tumor targets is not known. However, the mechanism does not appear to be related to a decrease in M phi viability.

Triglyceride-lowering effect of dietary vitamin E in streptozocin-induced diabetic rats. Increased lipoprotein lipase activity in livers of diabetic rats fed high dietary vitamin E.

High vitamin E supplementation in the diets of streptozocin-induced diabetic rats eliminates accumulation of lipid peroxides in the plasma and the liver, returns the plasma triglycerides toward normal levels, and increases the activity of lipoprotein lipase. Vitamin E has no effect on the levels of insulin or glucose. These findings suggest that vitamin E increases the total hepatic triglyceride lipase activity by increasing the lipoprotein lipase activity possibly by protecting the membrane-bound lipase against peroxidative damage.

Relation of left ventricular function and prognosis in hypertrophic cardiomyopathy: an angiographic study.

Left ventricular cineangiograms performed at the time of diagnosis in 88 patients with hypertrophic cardiomyopathy were digitized to evaluate the relation of left ventricular function and prognosis in hypertrophic cardiomyopathy. Eleven patients died suddenly after a mean follow-up period of 7.5 +/- 7 years, 10 patients died of congestive heart failure or after cardiac surgery and 67 were alive after a mean follow-up period of 8.6 +/- 4 years. Measurements of left ventricular volume, ejection fraction, peak rate of ejection and filling and time to peak rate of ejection and filling were derived from curves of ventricular volume and its rate of change during the cardiac cycle. Patients who died suddenly had a lower peak rate of ventricular ejection (stroke volume-normalized peak ejection rate 5.41 +/- 0.69 versus 6.24 +/- 1.33 s-1; p = 0.006) and lower peak rate of ventricular filling (end-diastolic volume-normalized peak filling rate 4.02 +/- 0.94 versus 4.88 +/- 1.53 s-1; p = 0.02) and stroke volume-normalized peak filling rate (4.75 +/- 1.08 versus 5.82 +/- 1.70 s-1; p = 0.01) compared with survivors. Stepwise regression analysis revealed that sudden death was best predicted by the combination of increased end-diastolic volume, small end-systolic volume and low peak filling rate (predictive accuracy 32%, false negative 18% and false positive 28%). The addition of clinical features and hemodynamic measurements to the analysis improved predictive accuracy to 43% (false negative 18% and false positive 18%). Ambulatory electrocardiographic monitoring performed in 57 of the 88 patients 1 month to 17 years (median 8 years) after diagnosis revealed ventricular tachycardia in 14 (25%). Of these, 10 who survived had hyperkinetic systolic function at diagnosis, whereas the 4 who died suddenly had impaired systolic function (end-diastolic volume-normalized peak ejection rate 5.93 +/- 1.2 versus 4.01 +/- 1.2 s-1, respectively; p = 0.04). In hypertrophic cardiomyopathy, ventricular tachycardia is a sensitive but nonspecific marker of adults who are at risk of sudden death. Impaired systolic function may be an important determinant of which patients with ventricular tachycardia die suddenly. This study shows that indexes of ventricular function contribute to the identification of patients at particular risk of sudden death. However, the predictive power of the clinical features and hemodynamic and angiographic measurements that could be assessed was poor.(ABSTRACT TRUNCATED AT 400 WORDS)

Behavioral Effects of Reducing the Daily Frequency of Phenothiazine Administration.

After an 11-day base line of behavioral observations, 24 chronic female schizophrenics were assigned to two groups matched for alertness. In the first treatment phase, the administration of phenothiazine medication of one group was switched from a multiple-dose schedule (three to four times per day) to a single daily administration, while the total dosage per day was held constant. The second group continued on a multiple administration schedule for 11 days and then was switched to a single daily dosage. A multivariate analysis of variance showed that there was no overall effect (positive or negative) due to the schedule change; however, preplanned t tests showed transitory decreases in nonfunctional behavior. The results are discussed in terms of implications for the administration of phenothiazines and the experimental analysis of drug effects.

Both hypothyroidism and hyperthyroidism enhance low density lipoprotein oxidation.

Hypothyroidism is frequently associated with hypercholesterolemia and an increased risk for atherosclerosis, whereas hyperthyroidism is known to precipitate angina or myocardial infarction in patients with underlying coronary heart disease. We have shown previously that L-T4 functions as an antioxidant in vitro and inhibits low density lipoprotein (LDL) oxidation in a dose-dependent fashion. The present study was designed to evaluate the changes in LDL oxidation in subjects with hypothyroidism and hyperthyroidism. Fasting blood samples for LDL oxidation analyses, lipoprotein determinations, and thyroid function tests were collected at baseline and after the patients were rendered euthyroid. The lag phase (mean +/- SEM hours) of the Cu+2-catalyzed LDL oxidation in the hypothyroid state and the subsequent euthyroid states were 4 +/- 0.0.65 and 14 +/- 0.68 h, respectively (P < 0.05). The lag phase during the hyperthyroid phase was 6 +/- 0.55 h, and that during the euthyroid phase was 12 +/- 0.66 h (P < 0.05). The total and LDL cholesterol levels were higher in hypothyroidism than in euthyroidism and were lower in hyperthyroidism than in the euthyroid state. We conclude that LDL has more susceptibility to oxidation in both the hypothyroid and hyperthyroid states. Thus, the enhanced LDL oxidation may play a role in the cardiac disease process in both hypothyroidism and hyperthyroidism.

Effects of nicotinic acid therapy on plasma lipoproteins and very low density lipoprotein apoprotein C subspecies in hyperlipoproteinemia.

The effects of long term treatment with nicotinic acid on lipids, lipoproteins, and the plasma distribution of very low density lipoproteins (VLDL) apoprotein C (ApoC) subspecies were studied in 33 patients with types IIa (n = 9), IIb (n = 11), and IV (n = 13) hyperlipidemias. After 6 months of treatment, a significant decrease in triglyceride, total cholesterol, and low density lipoprotein (LDL) cholesterol levels occurred. High density lipoprotein (HDL) cholesterol increased significantly by 31.1%, 41.8%, and 32.0% in types IIa, IIb, and IV, respectively (P less than 0.01 for all). A significant negative correlation existed between changes in HDL cholesterol and triglycerides (r = -0.613; P less than 0.02) in all groups studied. Therapy also produced changes in VLDL, LDL, and HDL protein concentrations. VLDL protein decreased from 20.9 +/- 3.9 to 15.2 +/- 1.0 mg/dl (P less than 0.05) in type IIa. In types IIb and IV, mean VLDL protein decreased from 44.7 +/- 8.2 to 27.1 +/- 3.9 mg/dl (P less than 0.001) and from 46.3 +/- 7.1 to 30.6 +/- 4.9 mg/dl (P less than 0.001), respectively. LDL protein decreased significantly, and HDL protein increased in type IIa only. Gel isoelectric focusing of VLDL before and after nicotinic acid in types IIb and IV hyperlipidemia produced a significant increase in the VLDL ApoC-II component with simultaneous decreases in the total VLDL ApoC-III subspecies. This resulted in increases in the ApoC-II to ApoC-III area ratio from 0.50 +/- 0.1 to 1.02 +/- 0.2 (P less than 0.001) in type IIb and from 0.62 +/- 0.07 to 0.88 +/- 0.13 (P less than 0.01) in type IV, respectively. The ApoE subspecies and the ApoE-III to ApoE-II area ratio did not change significantly. Our results show that nicotinic acid produces a significant improvement in the lipoprotein profiles of these patients.

Serum lipoprotein responses during active and stable weight reduction in reproductive obese females.

An increase in high density lipoprotein-cholesterol (HDL-C) and a reduction in low density lipoprotein-cholesterol (LDL-C) accompany weight reduction in obese males. In contrast, obese females have had variable responses in these two lipoproteins after weight reduction. To evaluate the effects of weight reduction in obese women, 15 morbidly obese eugonadotropic women of reproductive age had serum lipids and lipoproteins measured before and after achieving a stable and reduced weight by either diet and/or a gastric stapling procedure. Total testosterone (T), free testosterone (free T), and testosterone-binding globulin serum concentrations were also determined before and after achieving a stable reduced weight to assess the role of androgens in modulating any lipoprotein changes. In 10 subjects, lipid analysis was also performed during active weight loss. Total serum triglycerides fell from 106 +/- 53 to 76 +/- 30 mg/dl during active weight loss (P less than 0.025). Total cholesterol, LDL-C, HDL-C, and the LDL-C to HDL-C ratio did not change. In contrast, after achieving a stable reduced weight (mean weight reduction, 25.9 +/- 6.7 kg), HDL-C rose from 24 +/- 8 to 32 +/- 9 mg/dl (P less than 0.005). This was accompanied by a reduction in LDL-C from 145 +/- 23 to 135 +/- 30 mg/dl (P less than 0.01) and in the LDL-C to HDL-C ratio from 6.7 +/- 2.6 to 4.8 +/- 1.9 (P less than 0.001). Total triglycerides and total cholesterol were unchanged. After obtaining a stable reduced weight, testosterone-binding globulin increased and free T fell, but no significant correlation existed between the changes in androgens and the changes in lipoprotein responses. Thus, in morbidly obese women, weight reduction increases HDL-C and lowers LDL-C serum concentrations. The reduction in the LDL-C to HDL-C ratio suggests that weight loss may favorably reduce the risk of coronary artery disease in these patients. A concurrent reduction of free T with weight loss does not appear to be a major controlling influence in these lipoprotein alterations.

Brotizolam, a triazolothienodiazepine, in insomnia.

Sixty-three outpatients with chronic insomnia were treated for 3 weeks under double-blind conditions with either brotizolam (n = 29) at a dose of 0.25 mg or 0.5 mg or placebo (n = 34). A 3-day placebo period preceded and followed the double-blind treatment phase. Brotizolam consistently produced significantly more sleep improvement than placebo but also more adverse effects. In those patients switched abruptly from brotizolam to placebo, rebound insomnia was observed, being most marked at the first post-brotizolam placebo night.

Effect of herbal mixture student Rasayana on lipoxygenase activity and lipid peroxidation.

Brain cellular functions are affected by free radicals. Arachidonic acid and its 12-lipoxygenase metabolites have been proposed as important in enhancing long-term potentiation associated with learning. It has been reported that Student Rasayana (SR), an herbal mixture, improves brain functions. In this study we evaluated the antioxidant capacity of SR and its effect on lipoxygenase activity. Both alcoholic and aqueous extracts of SR inhibited enzymatic- and nonenzymatic-induced microsomal lipid peroxidation in a concentration-dependent manner. The agent concentrations (micrograms/mL) that produced 50% inhibition (IC50) of enzymatic- and nonenzymatic-induced microsomal lipid peroxidation, respectively, were 99.1 +/- 3.9 and 1992.0 +/- 122.7 for the aqueous extract, and 17.7 +/- 0.9 and 646.7 +/- 79.7 for the alcoholic extract. The aqueous extract inhibited soyabean lipoxygenase (SLP)-induced LDL oxidation in a concentration-dependent manner (IC50: 515.5 +/- 11.5), whereas the alcoholic extract enhanced SLP-induced LDL oxidation. Simultaneous addition of aqueous and alcoholic extracts inhibited SLP-induced LDL oxidation. The alcoholic extract (but not the aqueous extract) enhanced the ability of SLP to induce oxidation of linoleic acid. Rats fed 2% (w:w) SR showed inhibition of toluene-induced brain microsomal lipid peroxidation. These results suggest SR improves brain functions through scavenging free radicals as well as increasing the second messenger for long-term potentiation.

Direct spinal projections to limbic and striatal areas: anterograde transport studies from the upper cervical spinal cord and the cervical enlargement in squirrel monkey and rat.

With the anterograde tracers Phaseolus vulgaris-leucoagglutinin (PHA-L) and biotinylated dextranamine (BD), direct spinal connections from the upper cervical spinal cord (UC; C1 and C2) and the cervical enlargement (CE; C5-T1) were demonstrated in various striatal and limbic nuclei in both squirrel monkey and rat. Within each species and from each spinal level, the total number of terminals seen in the limbic and striatal areas was approximately 50-80% of the number seen within the thalamus. Labeled terminal structures were seen in the hypothalamic nuclei, ventral striatum, globus pallidus, amygdala, preoptic area, and septal nuclei. In both species, the number of labeled terminals in limbic and striatal regions was larger from UC than from CE, although the distributions to each nucleus varied with the specific lamina injected. In both species and from both UC and CE, approximately one-half of the projections to striatal and limbic areas terminated in the hypothalamus. The only region that demonstrated a topographical organization was the globus pallidus, where terminals from the CE were located dorsomedially to those from the UC. In the rat, UC and CE injections into the lateral dorsal horn and pericentral laminae resulted in the largest number of limbic and striatal terminations. The proportion of ipsilateral terminations was greatest when the medial laminae in the UC or the lateral dorsal horn in the CE received injections. Analysis of the morphology of these spinohypothalamic and spinotelencephalic terminals showed that, in the squirrel monkey, terminals from CE injections were larger than terminals from UC injections; no such size difference was evident in the rat. However, limbic and striatal terminals in the rat were generally larger than those in the squirrel monkey following injections into the UC or CE. The exact function of these direct spinal projections to various striatal and limbic areas in primates and in rodents remains to be determined. These findings, however, support recent imaging studies that suggest that the limbic system plays an important role in the mediation of chest pain, perhaps directly through these spinolimbic and spinostriatal pathways.

Glycemic index of foods: a physiological basis for carbohydrate exchange.

The determine the effect of different foods on the blood glucose, 62 commonly eaten foods and sugars were fed individually to groups of 5 to 10 healthy fasting volunteers. Blood glucose levels were measured over 2 h, and expressed as a percentage of the area under the glucose response curve when the same amount of carbohydrate was taken as glucose. The largest rises were seen with vegetables (70 +/- 5%), followed by breakfast cereals (65 +/- 5%), cereals and biscuits (60 +/- 3%), fruit (50 +/- 5%), dairy products (35 +/- 1%), and dried legumes (31 +/- 3%). A significant negative relationship was seen between fat (p less than 0.01) and protein (p less than 0.001) and postprandial glucose rise but not with fiber or sugar content.

Subjective effects of 3,4-methylenedioxymethamphetamine in recreational users.

3,4-Methylenedioxymethamphetamine (MDMA; Ecstasy) is a serotonergic neurotoxin in laboratory animals that has been used for recreational purposes by humans. The subjective effects of this drug were determined in recreational users at a university campus. Of individuals who had admitted to using MDMA recreationally, 100 of 143 agreed to complete a detailed questionnaire concerning the subjective effects of this Schedule I compound. The most common effect of MDMA was a heightened sense of "closeness" with other people (90% of subjects). Tachycardia, dry mouth, bruxism and/or trismus were reported by the majority of users. These effects probably result from the amphetaminelike properties of the drug. Visual hallucinations were reported by 20% of users. Untoward side effects were most common on the day following the use of MDMA, with complaints of muscle aches, fatiguability, depression, and difficulty concentrating noted by 21% to 36% of subjects. Sixty-seven percent of frequent users of the drug (six or more separate doses) reported that the "positive" effects of the drug decreased with successive doses while the "negative" effects increased. Although these observations should be considered preliminary, they represent the first documentation of the subjective effects of MDMA in recreational users and confirm previous reports obtained from patients treated with this drug.

Effects of pure capsaicinoids (capsaicin and dihydrocapsaicin) on plasma lipid and lipoprotein concentrations of turkey poults.

The effects of capsaicin and dihydrocapsaicin on blood lipid and lipoprotein concentrations were determined in two groups of turkeys. The first group was maintained on a cholesterol-free diet, while the second received a diet supplemented with 0.2% cholesterol. Daily administration of capsaicinoids occurred at a dose of 4 mg per animal. Neither drug had an effect on serum triglyceride concentrations in the animals receiving the cholesterol-free diet. However, total cholesterol, LDL-cholesterol and HDL-cholesterol concentrations were increased significantly, while VLDL cholesterol concentrations were decreased significantly by both drugs relative to controls. In the cholesterol-fed group triglycerides, total cholesterol and LDL-cholesterol decreased significantly with dihydrocapsaicin treatment. Both compounds reduced VLDL-cholesterol and increased HDL-cholesterol in the cholesterol-fed animals. Dihydrocapsaicin had a greater efficacy in producing beneficial anti-hyperlipidemic effects in the cholesterol-fed animals.