Monthly Archives: February 2012

Best Choices from the People’s Pharmacy is a book written by Joe Graedon and Terry Graedon, founders of The People’s Pharmacy. As with my post on their later book The People’s Pharmacy Quick and Handy Home Remedies, the notes in this post focus on treatments that have research backing from scientific studies. While this post focuses exclusively on natural remedies, the book also has useful information on prescription medications.

B Vitamins: reduce nighttime leg cramps

Bitter Melon: lowers fasting blood sugar

Boswellia: has anti-inflammatory effects, has anti-arthritic effects

Capsaicin: can protect the stomach lining

Cherries: inhibit inflammatory pathways, have some benefit against gout and arthritis

Chromium: may improve glucose tolerance in type 2 diabetics

Cinnamon (Cassia): lowers blood sugar, raises HDL cholesterol, reduces triglycerides

Coenzyme Q10: helps prevent migraines

Dark Chocolate: improves insulin sensitivity, lowers blood pressure, reduces the risk of heart disease, may reduce coughing

Fenugreek: can be used to treat type 1 and type 2 diabetes

Fish Oil: helpful in treating depression, may benefit patients with joint disease

Ginger: reduces knee pain

Grape Juice: raises good HDL cholesterol, reduces the oxidation of bad LDL cholesterol, diminishes platelet stickiness, reduces inflammation, lowers blood pressure

Grape Seed Extract: lowers blood pressure

Green-Lipped Mussel: improves arthritis symptoms

Green Tea: reduces the risk of hypertension

Gymnema Sylvestre: lowers blood sugar

Hemp Seed Oil: reduces itchiness and dryness in skin

Honey: active against Malassezia yeast

Magnesium: helps control blood pressure, helps prevent migraine headaches, helps maintain bone strength, reduces the risk of coronary heart disease, improves vascular function, improves heart pumping ability, improves sleep, helps treat restless leg syndrome

Melatonin: helps prevent migraines, improves sleep, prevents or reduces jet lag, helps treat tinnitus

MSM: may relieve pain

Niacin: lowers the risk of heart disease

Nopal: helps control blood sugar

Oolong Tea: lowers blood sugar, reduces symptoms of atopic dermatitis, reduces the risk of hypertension

Pomegranate: keeps bad LDL cholesterol from oxidizing, reduces inflammation in tissue cultures of human cartilage cells, may enhance oxygen flow to the heart in patients who have coronary artery disease, lowers blood pressure

Proanthocyanidins: reduce the risk of blood clots by making platelets less sticky while also making blood vessels more flexible

Probiotics: reduce stomach pain and bloating

Quercetin: stabilizes mast cells and makes them less likely to trigger the release of histamine and kinins

SAMe: may be as effective as NSAIDs in reducing pain and improving the condition of patients with osteoarthritis

Selenium: reduces the risk of developing arthritis

St. John’s Wort: effective in treating mild to moderate depression

Stevia: improves glucose tolerance

Stinging Nettle: reduces allergy symptoms, improves urine flow and decreases the amount of urine left in the bladder after voiding

Thyme: relieves congestion from colds

Turmeric: has anti-inflammatory effects, protects cartilage

Valerian: improves sleep quality

Vinegar: reduces blood sugar and insulin

Vitamin C: may help reduce allergy symptoms

Vitamin D: reduces the risk of colorectal/breast/ovarian cancer, reduces the risk of hip fracture, reduces the risk of osteoarthritis

Vitamin E: reduces symptoms of eczema

Zeaxanthin: reduces the risk of developing arthritis

Zinc: prevents bad breath, helps treat tinnitus

Antisocial personality disorder is a behavior disorder associated with aggression towards others. Psychopathy and antisocial personality disorder may be on a continuum of behavior, with psychopaths having a more extreme form of antisocial personality disorder. This post links to studies that describe the neurological, genetic, and physiological traits found in people with antisocial personality disorder or who exhibit antisocial behavior. A different set of studies that specifically focus on psychopathy can be found in the post The Science of Psychopaths.

• A gene x gene interaction between DRD2 and DRD4 is associated with conduct disorder and antisocial behavior in males. (Link)

• A longitudinal behavioral genetic analysis of the etiology of aggressive and nonaggressive antisocial behavior. (Link)

• A meta-analytic review of the relation between antisocial behavior and neuropsychological measures of executive function. (Link)

• A multivariate twin study of the DSM-IV criteria for antisocial personality disorder. (Link)

• A non-additive interaction of a functional MAO-A VNTR and testosterone predicts antisocial behavior. (Link)

• A pilot study revealing impaired P50 gating in antisocial personality disorder. (Link)

• A polymorphism of the MAOA gene is associated with emotional brain markers and personality traits on an antisocial index. (Link)

• A replicated molecular genetic basis for subtyping antisocial behavior in children with attention-deficit/hyperactivity disorder. (Link)

• Aggression as a mediator of genetic contributions to the association between negative parent-child relationships and adolescent antisocial behavior. (Link)

• Altered affective modulation of the startle reflex in alcoholics with antisocial personality disorder. (Link)

• An orbitofrontostriatopallidal pathway for morality: evidence from postlesion antisocial and obsessive-compulsive disorder. (Link)

• Antisocial personality disorder, childhood delinquency, and frontal brain functioning: EEG and neuropsychological findings. (Link)

• Antisocial symptoms in preadolescent boys and in their parents: associations with cortisol. (Link)

• Antisocial violent offenders with attention deficit hyperactivity disorder demonstrate akathisia-like hyperactivity in three-channel actometry. (Link)

• Anxiety, antisocial behavior, and heart rate regulation in adolescent males. (Link)

• Are there meaningful etiological differences within antisocial behavior? Results of a meta-analysis. (Link)

• Association analysis of 15 polymorphisms within 10 candidate genes for antisocial behavioural traits. (Link)

• Association of 5-HT1B receptor gene and antisocial behavior in alcoholism. (Link)

• Association of a regulatory polymorphism in the promoter region of the monoamine oxidase A gene with antisocial alcoholism. (Link)

• Association of COL25A1 with Comorbid Antisocial Personality Disorder and Substance Dependence. (Link)

• Case report: acquired antisocial personality disorder associated with unilateral left orbital frontal lobe damage. (Link)

• Catechol O-methyltransferase gene variant and birth weight predict early-onset antisocial behavior in children with attention-deficit/hyperactivity disorder. (Link)

• COMT polymorphisms in impulsively violent offenders with antisocial personality disorder. (Link)

• Corticotropin-releasing hormone and cortisol: longitudinal associations with depression and antisocial behavior in pregnant adolescents. (Link)

• Cortisol and alpha amylase reactivity and timing of puberty: vulnerabilities for antisocial behaviour in young adolescents. (Link)

• CSF 5-HIAA and family history of antisocial personality disorder in newborns. (Link)

• Development of antisocial disorders–impact of the autonomic stress system. (Link)

• Developmental structure of genetic influences on antisocial behavior across childhood and adolescence. (Link)

• Deviant peer affiliation and antisocial behavior: interaction with Monoamine Oxidase A (MAOA) genotype. (Link)

• Different allele distribution of a regulatory MAOA gene promoter polymorphism in antisocial and anxious-depressive alcoholics. (Link)

• Differential heritability of adult and juvenile antisocial traits. (Link)

• Do aggressive and non-aggressive antisocial behaviors in adolescents result from the same genetic and environmental effects? (Link)

• Effects of induced anger in patients with antisocial personality disorder. (Link)

• Effects of low birth weight, maternal smoking in pregnancy and social class on the phenotypic manifestation of Attention Deficit Hyperactivity Disorder and associated antisocial behaviour: investigation in a clinical sample. (Link)

• Electroencephalographic abnormalities in antisocial personality disorder. (Link)

• Energy substrate metabolism among habitually violent alcoholic offenders having antisocial personality disorder. (Link)

• Executive cognitive functioning, temperament, and antisocial behavior in conduct-disordered adolescent females. (Link)

• Exploring epistasis in candidate genes for antisocial personality disorder. (Link)

• Family dysfunction interacts with genes in the causation of antisocial symptoms. (Link)

• Free L-tryptophan plasma levels in antisocial violent offenders. (Link)

• Frontal brain dysfunction in alcoholism with and without antisocial personality disorder. (Link)

• Frontal P300 decrements in antisocial personality disorder. (Link)

• Functional imaging of conditioned aversive emotional responses in antisocial personality disorder. (Link)

• Gene environment interactions with a novel variable Monoamine Oxidase A transcriptional enhancer are associated with antisocial personality disorder. (Link)

• Genetic and cultural transmission of antisocial behavior: an extended twin parent model. (Link)

• Genetic and environmental bases of childhood antisocial behavior: a multi-informant twin study. (Link)

• Genetic and environmental influences on antisocial behavior: a meta-analysis of twin and adoption studies. (Link)

• Genetic and environmental influences on juvenile antisocial behaviour assessed on two occasions. (Link)

• Genetic contributions to antisocial personality and behavior: a meta-analytic review from an evolutionary perspective. (Link)

• Genetic contributions to continuity, change, and co-occurrence of antisocial and depressive symptoms in adolescence. (Link)

• Genetic influences on the overlap between low IQ and antisocial behavior in young children. (Link)

• Genotype link with extreme antisocial behavior: the contribution of cognitive pathways. (Link)

• Haplotypes of dopamine and serotonin transporter genes are associated with antisocial personality disorder in alcoholics. (Link)

• Heritability for adolescent antisocial behavior differs with socioeconomic status: gene-environment interaction. (Link)

• Homovanillic acid and dopamine-beta-hydroxylase in male youth: relationships with paternal substance abuse and antisocial behavior. (Link)

• HTR3B is associated with alcoholism with antisocial behavior and alpha EEG power–an intermediate phenotype for alcoholism and co-morbid behaviors. (Link)

• Improvement of aggressive and antisocial behavior after resection of temporal lobe tumors. (Link)

• Increased height and bulk in antisocial personality disorder and its subtypes. (Link)

• Incremental effect for antisocial personality disorder genetic risk combining 5-HTTLPR and 5-HTTVNTR polymorphisms. (Link)

• Interaction between ALDH2*1*1 and DRD2/ANKK1 TaqI A1A1 genes may be associated with antisocial personality disorder not co-morbid with alcoholism. (Link)

• Interaction of prenatal exposure to cigarettes and MAOA genotype in pathways to youth antisocial behavior. (Link)

• Latent class analysis of antisocial behavior: interaction of serotonin transporter genotype and maltreatment. (Link)

• Limbic responses to reward cues correlate with antisocial trait density in heavy drinkers. (Link)

• Linkage of antisocial alcoholism to the serotonin 5-HT1B receptor gene in 2 populations. (Link)

• MAOA, abuse exposure and antisocial behaviour: 30-year longitudinal study. (Link)

• Maternal prenatal smoking, parental antisocial behavior, and early childhood physical aggression. (Link)

• Maternal smoking during pregnancy and severe antisocial behavior in offspring: a review. (Link)

• Mediation of sensation seeking and behavioral inhibition on the relationship between heart rate and antisocial behavior: the TRAILS study. (Link)

• Moderating role of the MAOA genotype in antisocial behaviour. (Link)

• Monoamine oxidase A regulates antisocial personality in whites with no history of physical abuse. (Link)

• Neural and behavioural responses to threat in men with a history of serious violence and schizophrenia or antisocial personality disorder. (Link)

• Neurocognitive function in antisocial personality disorder. (Link)

• Neurocognitive impairments in boys on the life-course persistent antisocial path. (Link)

• Neurological soft signs in homicidal men with antisocial personality disorder. (Link)

• Neuronal correlates and serotonergic modulation of behavioural inhibition and reward in healthy and antisocial individuals. (Link)

• Nucleotide sequence variation within the human tyrosine kinase B neurotrophin receptor gene: association with antisocial alcohol dependence. (Link)

• Parenting and adolescent antisocial behavior and depression: evidence of genotype x parenting environment interaction. (Link)

• Preliminary evidence that specific candidate genes are associated with adolescent-onset antisocial behavior. (Link)

• Psychophysiological profiles of batterers: autonomic emotional reactivity as it predicts the antisocial spectrum of behavior among intimate partner abusers. (Link)

• Qualitative and quantitative EEG abnormalities in violent offenders with antisocial personality disorder. (Link)

• Quantitative electroencephalographic measures in homicidal men with antisocial personality disorder. (Link)

• Reduced prefrontal gray matter volume and reduced autonomic activity in antisocial personality disorder. (Link)

• Regional cortical thinning in subjects with violent antisocial personality disorder or schizophrenia. (Link)

• Relationship between antisocial behavior and regional cerebral blood flow in frontotemporal dementia. (Link)

• Resting cardiovascular activity and antisocial behavior in Essential and Reactive alcoholic men. (Link)

• Resting heart rate and the development of antisocial behavior from age 9 to 14: genetic and environmental influences. (Link)

• Risky decisions and their consequences: neural processing by boys with Antisocial Substance Disorder. (Link)

• Role of sex hormone-binding globulin in the relationship between sex hormones and antisocial and aggressive personality in inmates. (Link)

• Roles of perinatal problems on adolescent antisocial behaviors among children born after 33 completed weeks: a prospective investigation. (Link)

• Serotonergic function in children with attention-deficit hyperactivity disorder: relationship to later antisocial personality disorder. (Link)

• Sex differences in orbitofrontal gray as a partial explanation for sex differences in antisocial personality. (Link)

• Sex differences in the genetic and environmental influences on childhood conduct disorder and adult antisocial behavior. (Link)

• Single photon emission computerised tomography in chronic alcoholism. Antisocial personality disorder may be associated with decreased frontal perfusion. (Link)

• Spatial but not verbal cognitive deficits at age 3 years in persistently antisocial individuals. (Link)

• Strong genetic effects on cross-situational antisocial behaviour among 5-year-old children according to mothers, teachers, examiner-observers, and twins’ self-reports. (Link)

• Structural and functional MRI- findings in children and adolescents with antisocial behavior. (Link)

• Surface dental enamel lead levels and antisocial behavior in Brazilian adolescents. (Link)

• Swedish twin study surveys how antisocial behavior is developed. Hereditary factors are more important in girls, in older children and in aggressive behavior. (Link)

• Synaptosomal-associated protein 25 gene polymorphisms and antisocial personality disorder: association with temperament and psychopathy. (Link)

• Testing for gene x environment interaction effects in attention deficit hyperactivity disorder and associated antisocial behavior. (Link)

• The A1 allele of the DRD2 gene (TaqI A polymorphisms) is associated with antisocial personality in a sample of alcohol-dependent patients. (Link)

• The association between DRD2/ANKK1, 5-HTTLPR gene, and specific personality trait on antisocial alcoholism among Han Chinese in Taiwan. (Link)

• The association of 5-HTR2A-1438A/G, COMTVal158Met, MAOA-LPR, DATVNTR and 5-HTTVNTR gene polymorphisms and antisocial personality disorder in male heroin-dependent Chinese subjects. (Link)

• The development of antisocial behaviour from childhood to adolescence. A longitudinal twin study. (Link)

• The genetic and environmental etiology of antisocial behavior from childhood to emerging adulthood. (Link)

• The genetics of antisocial behavior. (Link)

• The neuropsychology of antisocial personality disorder. (Link)

• Tonic heart rate level, social class and antisocial behaviour in adolescents. (Link)

• Unraveling the effect of genes and environment in the transmission of parental antisocial behavior to children’s conduct disturbance, depression and hyperactivity. (Link)

• Volumetric structural brain abnormalities in men with schizophrenia or antisocial personality disorder. (Link)

• White matter microstructural abnormalities in the frontal lobe of adults with antisocial personality disorder. (Link)

This post links to studies that discuss the neurological traits, genes, and physiological features associated with psychopathy. There are genetic and environmental influences that cause people to develop psychopathic traits and predispose them to criminality. This means that certain areas of cities and nations may turn into breeding grounds for psychopaths when people with callous personalities reproduce and abuse their offspring. The study of psychopathy is therefore an important area of research for law enforcement, public health, and national defense.

• A biosocial interaction between prenatal exposure to cigarette smoke and family structure in the prediction of psychopathy in adolescence. (Link)

• A brain imaging (single photon emission computerized tomography) study of semantic and affective processing in psychopaths. (Link)

• A cognitive neuroscience perspective on psychopathy: evidence for paralimbic system dysfunction. (Link)

• A common genetic factor explains the association between psychopathic personality and antisocial behavior. (Link)

• A genetic factor explains most of the variation in the psychopathic personality. (Link)

• A neurophysiological dissociation between monitoring one’s own and others’ actions in psychopathy. (Link)

• A somatic marker perspective of immoral and corrupt behavior. (Link)

• Aberrant neural processing of moral violations in criminal psychopaths. (Link)

• Aberrant paralimbic gray matter in criminal psychopathy. (Link)

• Aberrant social and cerebral responding in a competitive reaction time paradigm in criminal psychopaths. (Link)

• Abnormal hippocampal shape in offenders with psychopathy. (Link)

• Abnormal structural correlates of response perseveration in individuals with psychopathy. (Link)

• Abnormal temporal and prefrontal cortical gray matter thinning in psychopaths. (Link)

• Abnormal ventromedial prefrontal cortex function in children with psychopathic traits during reversal learning. (Link)

• Abnormalities in emotion processing within cortical and subcortical regions in criminal psychopaths: evidence from a functional magnetic resonance imaging study using pictures with emotional content. (Link)

• Adolescents with psychopathic traits report reductions in physiological responses to fear. (Link)

• Aggression, psychopathy and brain imaging – Review and future recommendations. (Link)

• Altered connections on the road to psychopathy. (Link)

• Amygdala hypoactivity to fearful faces in boys with conduct problems and callous-unemotional traits. (Link)

• Association in alcoholic patients between psychopathic traits and the additive effect of allelic forms of the CNR1 and FAAH endocannabinoid genes, and the 3′ region of the DRD2 gene. (Link)

• Attention network performance and psychopathic symptoms in early adolescence: an ERP study. (Link)

• Attention to the eyes and fear-recognition deficits in child psychopathy. (Link)

• Autonomic stress reactivity and executive functions in successful and unsuccessful criminal psychopaths from the community. (Link)

• Behavioral effects of congenital ventromedial prefrontal cortex malformation. (Link)

• Behavioral evidence of prolonged interhemispheric transfer time among psychopathic offenders. (Link)

• Behavioral genetics in antisocial spectrum disorders and psychopathy: a review of the recent literature. (Link)

• Brain anatomy of persistent violent offenders: more rather than less. (Link)

• Brain circuits involved in emotional learning in antisocial behavior and social phobia in humans. (Link)

• Brain potentials implicate temporal lobe abnormalities in criminal psychopaths. (Link)

• Breakdown in the brain network subserving moral judgment in criminal psychopathy. (Link)

• Cardiac response and anxiety levels in psychopathic murderers. (Link)

• Corpus callosum abnormalities in psychopathic antisocial individuals. (Link)

• Cortex and amygdala morphology in psychopathy. (Link)

• Cortical correlates of impaired self-regulation in personality disordered patients with traits of psychopathy. (Link)

• CSF studies in violent offenders. I. 5-HIAA as a negative and HVA as a positive predictor of psychopathy. (Link)

• Default network deactivations are correlated with psychopathic personality traits. (Link)

• Defective somatic markers in sub-clinical psychopathy. (Link)

• Deficient fear conditioning in psychopathy: a functional magnetic resonance imaging study. (Link)

• Detecting psychopathy from thin slices of behavior. (Link)

• Differentiating among prefrontal substrates in psychopathy: neuropsychological test findings. (Link)

• Disentangling structural brain alterations associated with violent behavior from those associated with substance use disorders. (Link)

• Disrupted reinforcement signaling in the orbitofrontal cortex and caudate in youths with conduct disorder or oppositional defiant disorder and a high level of psychopathic traits. (Link)

• Disturbed prefrontal and temporal brain function during emotion and cognition interaction in criminal psychopathy. (Link)

• Divergent patterns of aggressive and neurocognitive characteristics in acquired versus developmental psychopathy. (Link)

• Do fearful eyes activate empathy-related brain regions in individuals with callous traits? (Link)

• DRD2 and ANKK1 genotype in alcohol-dependent patients with psychopathic traits: association and interaction study. (Link)

• Dual temperamental risk factors for psychopathic personality: evidence from self-report and skin conductance. (Link)

• Economic decision-making in psychopathy: a comparison with ventromedial prefrontal lesion patients. (Link)

• Elevated triiodothyronine in psychopathy – possible physiological mechanisms. (Link)

• Emotion disrupts neural activity during selective attention in psychopathy. (Link)

• Emotion in the criminal psychopath: fear image processing. (Link)

• Emotion in the criminal psychopath: startle reflex modulation. (Link)

• Emotional deficit in subjects with psychopathic tendencies as assessed by the Minnesota Multiphasic Personality Inventory-2: an event-related potentials study. (Link)

• Emotional processing in patients with a dissocial personality disorder subtype “psychopathy” according to PCL-R. (Link)

• ERPs on a continuous performance task and self-reported psychopathic traits: P3 and CNV augmentation are associated with Fearless Dominance. (Link)

• Evidence for substantial genetic risk for psychopathy in 7-year-olds. (Link)

• Evidence for unique threat-processing mechanisms in psychopathic and anxious individuals. (Link)

• Evidence of deviant emotional processing in psychopathy: a FMRI case study. (Link)

• Evoked potentials and psychopathy. (Link)

• Facial emotion processing in criminal psychopathy. Preliminary functional magnetic resonance imaging study. (Link)

• Functional differences among those high and low on a trait measure of psychopathy. (Link)

• Genetic and environmental influences on psychopathy trait dimensions in a community sample of male twins. (Link)

• Genetic and hormonal sensitivity to threat: Testing a serotonin transporter genotype×testosterone interaction. (Link)

• Genetic effects explain the stability of psychopathic personality from mid- to late adolescence. (Link)

• Genetic effects on male sexual coercion. (Link)

• Gray matter changes in right superior temporal gyrus in criminal psychopaths. Evidence from voxel-based morphometry. (Link)

• Heritable variations in gray matter concentration as a potential endophenotype for psychopathic traits. (Link)

• High psychopathic trait females exhibit reduced startle potentiation and increased p3 amplitude. (Link)

• Hippocampal structural asymmetry in unsuccessful psychopaths. (Link)

• Identification of psychopathic individuals using pattern classification of MRI images. (Link)

• Impairment of social and moral behavior related to early damage in human prefrontal cortex. (Link)

• In psychopathic patients emotion attribution modulates activity in outcome-related brain areas. (Link)

• In search of genes associated with risk for psychopathic tendencies in children: a two-stage genome-wide association study of pooled DNA. (Link)

• Increased testosterone-to-cortisol ratio in psychopathy. (Link)

• Increased volume of the striatum in psychopathic individuals. (Link)

• Inhibitory control and negative emotional processing in psychopathy and antisocial personality disorder. (Link)

• Investigating the neural correlates of psychopathy: a critical review. (Link)

• Limbic abnormalities in affective processing by criminal psychopaths as revealed by functional magnetic resonance imaging. (Link)

• Localization of deformations within the amygdala in individuals with psychopathy. (Link)

• Long-term validity of biological markers of psychopathy and criminal recidivism: follow-up 6-8 years after forensic psychiatric investigation. (Link)

• Magnetic resonance imaging volumetric analysis of the putamen in children with ADHD: combined type versus control. (Link)

• Mesolimbic dopamine reward system hypersensitivity in individuals with psychopathic traits. (Link)

• Morphological alterations in the prefrontal cortex and the amygdala in unsuccessful psychopaths. (Link)

• Neural correlates of error-related learning deficits in individuals with psychopathy. (Link)

• Neural correlates of social cooperation and non-cooperation as a function of psychopathy. (Link)

• Neural responses to emotional and neutral facial expressions in chronically violent men.  (Link)

• Neuroaffective processing in criminal psychopaths: brain event-related potentials reveal task-specific anomalies. (Link)

• Neurodevelopmental marker for limbic maldevelopment in antisocial personality disorder and psychopathy. (Link)

• Neuroendocrine responses to a glucose challenge in substance users with high and low levels of aggression, impulsivity, and antisocial personality. (Link)

• Neuroimaging in psychopathy. (Link)

• Neuroimaging of psychopathy and antisocial behavior: a targeted review. (Link)

• Neuropsychological implications of selective attentional functioning in psychopathic offenders. (Link)

• Neuroticism and psychopathy predict brain activation during moral and nonmoral emotion regulation. (Link)

• New evidence for an association between the CSF HVA:5-HIAA ratio and psychopathic traits. (Link)

• P3 event-related potential impairments in antisocial and psychopathic individuals: a meta-analysis. (Link)

• P3 event-related potentials and childhood maltreatment in successful and unsuccessful psychopaths. (Link)

• Personality correlates of physiological response to stress among incarcerated juveniles. (Link)

• Prefrontal structural and functional brain imaging findings in antisocial, violent, and psychopathic individuals: a meta-analysis. (Link)

• Psychopathic personality in children: genetic and environmental contributions. (Link)

• Psychopathic personality traits and cortisol response to stress: the role of sex, type of stressor, and menstrual phase. (Link)

• Psychopathic personality traits in middle-aged male twins: a behavior genetic investigation. (Link)

• Psychopathic personality traits: heritability and genetic overlap with internalizing and externalizing psychopathology. (Link)

• Psychopathic tendencies and mesolimbic recruitment by cues for instrumental and passively obtained rewards. (Link)

• Psychopathic traits and autonomic responding to concealed information in a prison sample. (Link)

• Psychopathic traits and deception: functional magnetic resonance imaging study. (Link)

• Psychopathic Traits and Physiological Responses to Aversive Stimuli in Children Aged 9-11 Years. (Link)

• Psychopathy and functional magnetic resonance imaging blood oxygenation level-dependent responses to emotional faces in violent patients with schizophrenia. (Link)

• Psychopathy and physiological response to emotionally evocative sounds. (Link)

• Psychopathy and the mirror neuron system: preliminary findings from a non-psychiatric sample. (Link)

• Psychopathy and the posterior hippocampus. (Link)

• Psychopathy as a disorder of the moral brain: fronto-temporo-limbic grey matter reductions demonstrated by voxel-based morphometry. (Link)

• Psychopathy trait scores in adolescents with childhood ADHD: the contribution of genotypes affecting MAOA, 5HTT and COMT activity. (Link)

• Psychopathy, startle blink modulation, and electrodermal reactivity in twin men. (Link)

• Psychophysiology of aggression, psychopathy, and conduct problems: a meta-analysis. (Link)

• Reduced amygdala-orbitofrontal connectivity during moral judgments in youths with disruptive behavior disorders and psychopathic traits. (Link)

• Reduced electrodermal activity in psychopathy-prone adolescents. (Link)

• Reduced electrodermal fear conditioning from ages 3 to 8 years is associated with aggressive behavior at age 8 years. (Link)

• Reduced frontotemporal perfusion in psychopathic personality. (Link)

• Reduced P300 responses in criminal psychopaths during a visual oddball task. (Link)

• Reduced prefrontal connectivity in psychopathy. (Link)

• Reduced susceptibility to the attentional blink in psychopathic offenders: Implications for the attention bottleneck hypothesis. (Link)

• Relationship between 5-HT function and impulsivity and aggression in male offenders with personality disorders. (Link)

• Relationships between N1, P300, and contingent negative variation recorded at age 15 and criminal behavior at age 24. (Link)

• Risky decisions and response reversal: is there evidence of orbitofrontal cortex dysfunction in psychopathic individuals? (Link)

• Self-reported trauma, cortisol levels, and aggression in psychopathic and non-psychopathic prison inmates. (Link)

• Semantic and affective processing in psychopaths: an event-related potential (ERP) study. (Link)

• Serotonergic and cognitive impairment in impulsive aggressive personality disordered offenders: are there implications for treatment? (Link)

• Serotonin transporter gene associations with psychopathic traits in youth vary as a function of socioeconomic resources. (Link)

• Serum levels of thyroid hormones as biological markers in a Swedish forensic psychiatric population. (Link)

• Sex-specific association between psychopathic traits and electrodermal reactivity in children. (Link)

• Size matters: increased grey matter in boys with conduct problems and callous-unemotional traits. (Link)

• Small, but not perfectly formed: decreased white matter concentration in boys with psychopathic tendencies. (Link)

• Startle reflex modulation, affective ratings and autonomic reactivity in incarcerated Spanish psychopaths. (Link)

• State-dependent executive deficits among psychopathic offenders. (Link)

• Structural brain abnormalities in psychopaths-a review. (Link)

• Symptoms of executive dysfunction are endemic to secondary psychopathy: an examination in criminal offenders and noninstitutionalized young adults. (Link)

• Temporal lobe abnormalities in semantic processing by criminal psychopaths as revealed by functional magnetic resonance imaging. (Link)

• Testosterone as a biological marker in psychopathy and alcoholism. (Link)

• The amygdala and ventromedial prefrontal cortex: functional contributions and dysfunction in psychopathy. (Link)

• The clinical EEG and personality in mentally abnormal offenders. (Link)

• The genetic and environmental covariation among psychopathic personality traits, and reactive and proactive aggression in childhood. (Link)

• The neurobiology of psychopathy: a neurodevelopmental perspective. (Link)

• The Neuropsychological Underpinnings to Psychopathic Personality Traits in a Nationally Representative and Longitudinal Sample. (Link)

• The other allele: exploring the long allele of the serotonin transporter gene as a potential risk factor for psychopathy: a review of the parallels in findings. (Link)

• The psychopath magnetized: insights from brain imaging. (Link)

• The role of the orbitofrontal cortex in affective theory of mind deficits in criminal offenders with psychopathic tendencies. (Link)

• Ventral frontal deficits in psychopathy: neuropsychological test findings. (Link)

• Visual P3 amplitude and self-reported psychopathic personality traits: frontal reduction is associated with self-centered impulsivity. (Link)

• Volume reduction in prefrontal gray matter in unsuccessful criminal psychopaths. (Link)

Borderline Personality Disorder is a mental condition involving problems with regulating emotions and actions. It can be distressing to patients and their families. This post links to studies discussing the involvement of neurological traits and behavioral genetics in BPD. This paper describes some potential psychopharmacological treatments.

• 5-HT1A receptor gene C -1019 G polymorphism and amygdala volume in borderline personality disorder. (Link)

• 5HT2A receptor binding is increased in borderline personality disorder. (Link)

• A brain MRI study in subjects with borderline personality disorder. (Link)

• A developmental neuroscience of borderline pathology: emotion dysregulation and social baseline theory. (Link)

• A fenfluramine-activated FDG-PET study of borderline personality disorder. (Link)

• A positron emission tomography study of memories of childhood abuse in borderline personality disorder. (Link)

• A voxel-based morphometric MRI study in female patients with borderline personality disorder. (Link)

• A voxel-based morphometric MRI study in men with borderline personality disorder: preliminary findings. (Link)

• Aberrant connectivity of resting-state networks in borderline personality disorder. (Link)

• Abnormal prefrontal cortical response during affective processing in borderline personality disorder. (Link)

• Alterations of symptoms with borderline personality disorder after fronto-temporal traumatic brain injury. A case study. (Link)

• Altered emotional information processing in borderline personality disorder: an electrophysiological study. (Link)

• Amygdala deactivation as a neural correlate of pain processing in patients with borderline personality disorder and co-occurrent posttraumatic stress disorder. (Link)

• Amygdala hyperreactivity in borderline personality disorder: implications for emotional dysregulation. (Link)

• Amygdala-prefrontal disconnection in borderline personality disorder. (Link)

• Amygdala volume and depressive symptoms in patients with borderline personality disorder. (Link)

• An investigation of organic factors in the neuropsychological functioning of patients with borderline personality disorder. (Link)

• An MRI study of pituitary volume and parasuicidal behavior in teenagers with first-presentation borderline personality disorder. (Link)

• Anatomical MRI study of borderline personality disorder patients. (Link)

• Anterior cingulate volume in adolescents with first-presentation borderline personality disorder. (Link)

• Anterior cingulate volume reduction in adolescents with borderline personality disorder and co-morbid major depression. (Link)

• Association analysis of serotonin receptor 1B (HTR1B) and brain-derived neurotrophic factor gene polymorphisms in Borderline personality disorder. (Link)

• Association between 5-HTTLPR and Borderline Personality Disorder Traits among Youth. (Link)

• Association between dopaminergic polymorphisms and borderline personality traits among at-risk young adults and psychiatric inpatients. (Link)

• Borderline personality disorder associated with psychotic symptoms and parietal lobe abnormalities. (Link)

• Borderline personality disorder features in adolescent girls: P300 evidence of altered brain maturation. (Link)

• Borderline personality features possibly related to cingulate and orbitofrontal cortices dysfunction due to schizencephaly. (Link)

• Borderline personality disorder: hypothalamus pituitary adrenal axis and findings from neuroimaging studies. (Link)

• Borderline personality disorder, impulsivity, and the orbitofrontal cortex. (Link)

• Borderline personality traits and adult attention-deficit hyperactivity disorder symptoms: a genetic analysis of comorbidity. (Link)

• Brain glucose metabolism in borderline personality disorder. (Link)

• Brain Regional alpha-[11C]methyl-L-tryptophan trapping in impulsive subjects with borderline personality disorder. (Link)

• Brain structure and function in borderline personality disorder. (Link)

• Chromosome 9: linkage for borderline personality disorder features. (Link)

• COMT val158met Polymorphism and Neural Pain Processing. (Link)

• Contribution of neurobiology to our knowledge of borderline personality disorder. (Link)

• Corpus callosum abnormalities in women with borderline personality disorder and comorbid attention-deficit hyperactivity disorder. (Link)

• Corpus callosum morphology and relationship to orbitofrontal and lateral ventricular volume in teenagers with first-presentation borderline personality disorder. (Link)

• Correlation of glutamate levels in the anterior cingulate cortex with self-reported impulsivity in patients with borderline personality disorder and healthy controls. (Link)

• Cortical inhibition in alexithymic patients with borderline personality disorder. (Link)

• Corticolimbic function in impulsive aggressive behavior. (Link)

• Deficits in visual functions and neuropsychological inconsistency in Borderline Personality Disorder. (Link)

• Defining the neurocircuitry of borderline personality disorder: functional neuroimaging approaches. (Link)

• Developmental pathways to borderline personality disorder. (Link)

• Dissociation and emotion regulation in borderline personality disorder. (Link)

• Distinct pattern of P3a event-related potential in borderline personality disorder. (Link)

• Dorso- and ventro-lateral prefrontal volume and spatial working memory in schizotypal personality disorder. (Link)

• Dorsolateral prefrontal cortex and hippocampus sustain impulsivity and aggressiveness in borderline personality disorder. (Link)

• Dysregulation of regional endogenous opioid function in borderline personality disorder. (Link)

• Dysregulation of the executive system and theory of mind: clinical interest of a neuroscientific conception of BPD. (Link)

• EEG theta activity and pain insensitivity in self-injurious borderline patients. (Link)

• EEG-vigilance differences between patients with borderline personality disorder, patients with obsessive-compulsive disorder and healthy controls. (Link)

• Effects of dialectic-behavioral-therapy on the neural correlates of affective hyperarousal in borderline personality disorder. (Link)

• Electroencephalographic abnormalities in borderline personality disorder. (Link)

• Electroencephalography of DSM-III borderline personality disorder. (Link)

• Emotionally controlled decision-making and a gene variant related to serotonin synthesis in women with borderline personality disorder. (Link)

• Evidence of abnormal amygdala functioning in borderline personality disorder: a functional MRI study. (Link)

• Evidence of disturbed amygdalar energy metabolism in patients with borderline personality disorder. (Link)

• Facial emotion triggered cerebral potentials in treatment-resistant depression and borderline personality disorder patients of both genders. (Link)

• Failure of frontolimbic inhibitory function in the context of negative emotion in borderline personality disorder. (Link)

• Familial resemblance of borderline personality disorder features: genetic or cultural transmission? (Link)

• First-cycle REM density in never-depressed subjects with borderline personality disorder. (Link)

• Frontal white matter integrity in borderline personality disorder with self-injurious behavior. (Link)

• Fronto-limbic dysfunction in borderline personality disorder: a 18F-FDG positron emission tomography study. (Link)

• Fronto-limbic dysfunction in response to facial emotion in borderline personality disorder: an event-related fMRI study. (Link)

• Frontolimbic brain abnormalities in patients with borderline personality disorder: a volumetric magnetic resonance imaging study. (Link)

• Frontolimbic structural changes in borderline personality disorder. (Link)

• Functional MRI correlates of the recall of unresolved life events in borderline personality disorder. (Link)

• Gender differences in a fenfluramine-activated FDG PET study of borderline personality disorder. (Link)

• Genetic covariance structure of the four main features of borderline personality disorder. (Link)

• Heritability of borderline personality disorder features is similar across three countries. (Link)

• Higher executive control and visual memory performance predict treatment completion in borderline personality disorder. (Link)

• Hippocampal volume in borderline personality disorder with and without comorbid posttraumatic stress disorder: a meta-analysis. (Link)

• Hippocampal volume reduction and history of aggressive behaviour in patients with borderline personality disorder. (Link)

• Hippocampus and amygdala volumes in patients with borderline personality disorder with or without posttraumatic stress disorder. (Link)

• Hormones and Borderline Personality Features. (Link)

• How neuroscience and behavioral genetics improve psychiatric assessment: report on a violent murder case. (Link)

• HPA axis alterations in mental disorders: impact on memory and its relevance for therapeutic interventions. (Link)

• [I-123] ADAM and SPECT in patients with borderline personality disorder and healthy control subjects. (Link)

• Impaired decision making and feedback evaluation in borderline personality disorder. (Link)

• Impulsivity and prefrontal hypometabolism in borderline personality disorder. (Link)

• Increased delta power and discrepancies in objective and subjective sleep measurements in borderline personality disorder. (Link)

• Increased DNA methylation of neuropsychiatric genes occurs in borderline personality disorder. (Link)

• Increased p50 gating but intact prepulse inhibition in borderline personality disorder. (Link)

• Inferior frontal white matter microstructure and patterns of psychopathology in women with borderline personality disorder and comorbid attention-deficit hyperactivity disorder. (Link)

• Insular cortex volume and impulsivity in teenagers with first-presentation borderline personality disorder. (Link)

• Interaction between gene variants of the serotonin transporter promoter region (5-HTTLPR) and catechol O-methyltransferase (COMT) in borderline personality disorder. (Link)

• Interaction between tryptophan hydroxylase I polymorphisms and childhood abuse is associated with increased risk for borderline personality disorder in adulthood. (Link)

• Interconnection between biological abnormalities in borderline personality disorder: use of the Bayesian networks model. (Link)

• Intima-media thickness in women with borderline personality disorder. (Link)

• Is borderline personality a particularly right hemispheric disorder? A study of P3a using single trial analysis. (Link)

• Laboratory induced aggression: a positron emission tomography study of aggressive individuals with borderline personality disorder. (Link)

• Magnetic resonance imaging of hippocampal and amygdala volume in women with childhood abuse and borderline personality disorder. (Link)

• Magnetic resonance imaging volumes of the hippocampus and the amygdala in women with borderline personality disorder and early traumatization. (Link)

• Medial prefrontal cortex hyperactivation during social exclusion in borderline personality disorder. (Link)

• Metabolic alterations in the amygdala in borderline personality disorder: a proton magnetic resonance spectroscopy study. (Link)

• Midline brain structures in teenagers with first-presentation borderline personality disorder. (Link)

• ”Missing links” in borderline personality disorder: loss of neural synchrony relates to lack of emotion regulation and impulse control. (Link)

• Monoamine oxidase a gene is associated with borderline personality disorder. (Link)

• Neural correlates of antinociception in borderline personality disorder. (Link)

• Neural correlates of attachment trauma in borderline personality disorder: a functional magnetic resonance imaging study. (Link)

• Neural correlates of emotion processing in borderline personality disorder. (Link)

• Neural correlates of episodic and semantic memory retrieval in borderline personality disorder: an fMRI study. (Link)

• Neural correlates of impaired emotional discrimination in borderline personality disorder: an fMRI study. (Link)

• Neural correlates of impulsive responding in borderline personality disorder: ERP evidence for reduced action monitoring. (Link)

• Neural correlates of memories of abandonment in women with and without borderline personality disorder. (Link)

• Neural correlates of the individual emotional Stroop in borderline personality disorder.  (Link)

• Neural correlates of the use of psychological distancing to regulate responses to negative social cues: a study of patients with borderline personality disorder. (Link)

• Neural processing of emotional overinvolvement in borderline personality disorder. (Link)

• Neurobehavioral study of borderline personality disorder. (Link)

• Neurobiological basis of parenting disturbance. (Link)

• Neurobiological substrates of antisocial and borderline personality disorder: preliminary results of a functional fMRI study. (Link)

• Neurochemical alterations in women with borderline personality disorder and comorbid attention-deficit hyperactivity disorder. (Link)

• Neurocognitive deficits in decision-making and planning of patients with DSM-III-R borderline personality disorder. (Link)

• Neurocognitive function in borderline personality disorder. (Link)

• Neuronal correlates of altered empathy and social cognition in borderline personality disorder. (Link)

• Neuronal correlates of cognitive reappraisal in borderline patients with affective instability. (Link)

• Neurocognitive functioning in borderline personality disorder. (Link)

• Neuroimaging and genetics of borderline personality disorder: a review. (Link)

• Neuroimaging in borderline personality disorder. (Link)

• Neuroimaging studies in borderline personality disorder. (Link)

• Neurologic soft signs in borderline personality disorder. (Link)

• Neuronal correlates of reward and loss in Cluster B personality disorders: a functional magnetic resonance imaging study. (Link)

• Neurophysiological correlates of borderline personality disorder: a transcranial magnetic stimulation study. (Link)

• Neuropsychobiological aspects, comorbidity patterns and dimensional models in borderline personality disorder. (Link)

• Neuropsychological dysfunctions in personality borderline disorder: detection strategies. (Link)

• Neuropsychological function in borderline personality disorder. (Link)

• Neuropsychological impairment in borderline personality disorder. (Link)

• Neuropsychological rehabilitation in patients with borderline personality disorder: a case series. (Link)

• One-year functional magnetic resonance imaging follow-up study of neural activation during the recall of unresolved negative life events in borderline personality disorder. (Link)

• Orbitofrontal, amygdala and hippocampal volumes in teenagers with first-presentation borderline personality disorder. (Link)

• Orbitofrontal dysfunction related to depressive symptomatology in subjects with borderline personality disorder. (Link)

• Pain sensitivity and neural processing during dissociative states in patients with borderline personality disorder with and without comorbid posttraumatic stress disorder: a pilot study. (Link)

• Pathological dissociation and neuropsychological functioning in borderline personality disorder. (Link)

• Pituitary volume in teenagers with first-presentation borderline personality disorder. (Link)

• Polysomnographic studies on sleep in adult borderline personality disorder. (Link)

• Positron-emission tomography and personality disorders. (Link)

• Positron emission tomography in female patients with borderline personality disorder. (Link)

• Positron emission tomography of regional brain metabolic responses to a serotonergic challenge in major depressive disorder with and without borderline personality disorder. (Link)

• Posttraumatic stress disorder and fMRI activation patterns of traumatic memory in patients with borderline personality disorder. (Link)

• Processing of visual stimuli in borderline personality disorder: a combined behavioural and magnetoencephalographic study. (Link)

• Psychobiology of borderline personality traits related to subtypes of eating disorders: a study of platelet MAO activity. (Link)

• Rare genotype combination of the serotonin transporter gene associated with treatment response in severe personality disorder. (Link)

• Reduced amygdala and hippocampus size in trauma-exposed women with borderline personality disorder and without posttraumatic stress disorder. (Link)

• Reduced anterior and posterior cingulate gray matter in borderline personality disorder. (Link)

• Reduced anterior cingulate and orbitofrontal volumes in child abuse-related complex PTSD. (Link)

• Reduced deactivation in reward circuitry and midline structures during emotion processing in borderline personality disorder. (Link)

• Reduced glucose metabolism in temporo-parietal cortices of women with borderline personality disorder. (Link)

• Reduced interhemispheric structural connectivity between anterior cingulate cortices in borderline personality disorder. (Link)

• Reduced prefrontal and orbitofrontal gray matter in female adolescents with borderline personality disorder: is it disorder specific? (Link)

• Reduced size and abnormal asymmetry of parietal cortex in women with borderline personality disorder. (Link)

• Repeat neurobehavioral study of borderline personality disorder. (Link)

• Script-driven imagery of self-injurious behavior in patients with borderline personality disorder: a pilot FMRI study. (Link)

• Selective deficit in executive functioning among patients with borderline personality disorder. (Link)

• Serotonin genes and gene-gene interactions in borderline personality disorder in a matched case-control study. (Link)

• Size abnormalities of the superior parietal cortices are related to dissociation in borderline personality disorder. (Link)

• Soft sign neurological abnormalities in borderline personality disorder and normal control subjects. (Link)

• Stability, change, and heritability of borderline personality disorder traits from adolescence to adulthood: a longitudinal twin study. (Link)

• Structural brain abnormalities and suicidal behavior in borderline personality disorder. (Link)

• Structural brain abnormalities in borderline personality disorder: a voxel-based morphometry study. (Link)

• Subtle prefrontal neuropathology in a pilot magnetic resonance spectroscopy study in patients with borderline personality disorder. (Link)

• Superior temporal gyrus volume in teenagers with first-presentation borderline personality disorder. (Link)

• Symptoms and EEG findings in the borderline syndrome. (Link)

• The catechol o-methyltransferase (COMT) val(158)met polymorphism modulates the association of serious life events (SLE) and impulsive aggression in female patients with borderline personality disorder (BPD). (Link)

• The five-factor model of personality and borderline personality disorder: a genetic analysis of comorbidity. (Link)

• The latest neuroimaging findings in borderline personality disorder. (Link)

• The neuropsychology of borderline personality disorder: a meta-analysis and review. (Link)

• The neuropsychology of borderline personality disorder: relationship with clinical dimensions and comparison with other personality disorders. (Link)

• The role of functional neuroimaging in exploring the overlap between borderline personality disorder and bipolar disorder. (Link)

• Tryptophan-hydroxylase 2 haplotype association with borderline personality disorder and aggression in a sample of patients with personality disorders and healthy controls. (Link)

• Variable number of tandem repeat polymorphisms of the arginine vasopressin receptor 1A gene and impulsive aggression in patients with borderline personality disorder. (Link)

• Volumes of the hippocampus and amygdala in patients with borderline personality disorder: a meta-analysis. (Link)

The Gene Smart Diet is a book by Dr. Floyd Chilton, a professor at Wake Forest University who also wrote Inflammation Nation. This post has some notes from the book. Gene Smart Wellness offers an omega 3 home blood test kit for individuals to check their level of inflammation.

• A study of the Gene Smart Diet found that participants lost an average of 1.5 to 2 pounds, 0.5 inches around their waists, and almost 0.5 percent of their body fat per week. The participants also showed marked reductions in their hemoglobin A1, HOMA, and SCD1, among other biomarkers of insulin resistance and diabetes. They also reduced fasting insulin levels by more than 30 percent. More than 90 percent of participants stayed on the program until the very end.

• Scientists have found very high levels of inflammatory messengers in people with depression.

• Mice engineered without the ability to produce the inflammatory messenger tumor necrosis factor alpha never developed tumors.

• A body mass index over 32 doubles the risk of death, mostly from inflammatory diseases like heart disease, cancer, stroke, and diabetes.

• A study showed that low leptin levels cause behavioral changes that make resisting food very difficult.

• Data collected from more than 20 studies demonstrate that higher than ordinary levels of C-reactive protein are strongly associated with nearly all of the important cardiovascular risk factors.

• According to three recent studies, C-reactive protein is an important determinant of both near-term and all-cause mortality.

• Tumor necrosis factor alpha is associated with insulin resistance, diabetes, hardening of the arteries, and congestive heart failure.

• A study of resveratrol in mice found that they were able to run twice as far as mice not given resveratrol.

• Resveratrol interferes with the three stages of cancer formation and modulates the master regulator NF-kB.

• An interventional study demonstrated that aerobic and resistance training reduced C-reactive protein levels in both old and young participants by 50 to 60 percent.

• A study found that women were more sexually responsive following 20 minutes of vigorous exercise.

• In males, short bouts of intense exercise have been linked with increased testosterone levels.

• The European Prospective Investigation into Cancer and Nutrition study found that in populations with low fiber intakes, doubling dietary fiber could reduce the colon cancer risk by 40 percent.

• The NHANES epidemiological study found that the more fiber people eat, the less likely they are to have high circulating concentrations of C-reactive protein.

• Some studies suggest that butyrate (a fatty acid found in fermentable fibers) may act as an anti-inflammatory.

• Fish oil can reduce predictors of heart disease such as high triglycerides and elevated resting heart rate.

• Fish oil supplements can reduce chances of death from a heart attack in people with a history of heart disease by as much as 50 percent.

• The GISSI-Prevenzione study of over 11,000 patients with a recent heart attack found that long-chain omega-3 PUFA supplements led to a 45 percent reduction in sudden cardiac death during the next 3.5 years.

• A study found that for each 20 grams a day (a little more than half an ounce) increase in fish consumption, there is an associated 7 percent reduction in fatal coronary heart disease.

• A study found that most cardiac and stroke events occur in individuals without elevated cholesterol.

• A study found that the administration of omega-3 fatty acids in critical-care settings significantly improved survival and diminished mortality, infection rates, and length of hospital stay.

• Six clinical trials have shown that the long-chain omega-3 EPA significantly improved depressive symptoms when compared with the placebo-treated population.

• In animal models of Alzheimer’s disease, dietary depletion of DHA dramatically worsens the disease, while DHA supplementation markedly improves cognitive function.

• A study of nearly 1,000 men found that those who consumed the largest amounts of omega-6 fats showed a 76 percent greater decline in general cognitive function than those who ate the lowest amounts.

• A study of 210 participants between 70 and 89 years of age found that those who consumed fish had significantly less cognitive decline over the intervening five years than those who didn’t eat fish.

• A study of Australian children found that those who were fed oily fish were 75 percent less likely to develop allergic asthma.

• A study in Japan found that long-chain omega-3 supplementation produced an improvement in asthmatic symptoms and a decrease in airway responsiveness.

• Research shows that shifting circulating rates of omega-6s to omega-3s from greater than 15:1 to less than 5:1 in humans turns down the genes that cause inflammation and allergy.

• A study found that fish oils improve lung function by 69 percent and reduce inflammatory messenger levels in respiratory fluids by greater than 70 percent in people with exercise-induced asthma.

• A study of patients with COPD found that those who received a long-chain omega-3 supplement significantly increased the rate at which they got oxygen.

• Numerous studies have shown that long-chain omega-3 fats lead to a decrease in NSAID requirements, decreases in morning stiffness, and decreases in the number of painful joints.

• The medium-chain omega-6 GLA found in borage oil has had clinical benefit similar to that of long-chain omega-3s.

• A study of patients hospitalized for acute psoriasis found that daily infusions of an omega-3 fatty acid-based lipid emulsion led to significant improvements in all score systems ranging between 45 percent and 76 percent within 10 days.

• A study showed that omega-3 fats reduce body fat by improving blood flow to muscles during exercise.

• A study showed that overweight people who supplemented with omega-3 fatty acids burned up to 26 percent more calories from fat than a placebo group and had half the insulin levels, markedly reducing their chance of insulin resistance and diabetes.

• A study found that mice fed resveratrol for 15 weeks had two times the treadmill endurance of a control group.

• A study of 340 people found that heart-attack risk declined by 44 percent in those drinking 1 cup or more of tea per day compared with nondrinkers.

• Platelets isolated from healthy human subjects show decrease aggregation when pretreated with red wine, grape juice, or resveratrol-enriched grape juice.

• Numerous human studies have shown that dark chocolate reduces blood pressure and improves insulin sensitivity.

• Polyphenols such as quercetin, catechins, resveratrol, caffeic acid, and anthocyanins reduce signs and symptoms of arthritis in animal models.

• A combination of quercetin and curcumin has been shown to reduce the number and size of tumors in patients with familial adenomatous polyposis, an inherited colorectal cancer.

The Doctor’s Heart Cure is a book by Dr. Al Sears, the director of an anti-aging clinic with 20,000 patients. The book describes research-based techniques for heart health. Dr. Sears also reveals the true story of Dr. Robert Atkins’ weight at the time of his death, an issue that has been controversial in the nutrition community. Apparently, Atkins was obese at the time of his death, but only from fluid retention and swelling resulting from corticosteroid drugs that were administered when he was hospitalized after falling on an icy surface. Dr. Atkins had been in good health and at a normal weight before his accident.

This post has some notes from the book.

• Studies of modern hunter-gatherer societies show that all derive more than half of their subsistence from animal foods.

• The high insulin levels brought on from excessive carbohydrate intake prevents the body from burning stored body fat for energy.

• A study found that patients on a very-low-carbohydrate diet lost significantly more weight than those on a low-fat, low-calorie diet in a six-month period. The low-carbohydrate group also lost more body fat than the low-fat group.

• A study that examined people eating very-low-fat diets concluded that there was no improvement in body composition, blood sugar levels, insulin levels, or blood pressure levels.

• A study found that people who eat low-fat diets develop weaker immune systems.

• A study found that the Atkins diet caused greater weight loss and lowered triglycerides much more effectively than the American Heart Association’s low-fat diet.

• A study found that men who did high-intensity interval exercise reduced their heart attack risk by 100 percent more than those who did endurance exercise.

• A study found that testosterone levels increase more in men who do interval exercise than in those doing endurance training.

• A study found that distance running disrupted the balance of blood thinners and thickeners, elevating clotting levels and inflammatory factors.

• A study found that many elderly participants who used walkers or wheelchairs were able to walk unaided after 10 weeks of muscle building exercise.

• A study in Switzerland found that there was not a statistically significant link between cholesterol and coronary artery disease.

• Nearly 75 percent of people who have heart attacks have normal cholesterol levels.

• Mexico has 2750 percent higher fat intake than Japan, yet only one-sixth the risk of heart disease.

• Results of the Framingham study showed that 80 percent of heart attack patients had similar lipid levels to those who did not have heart attacks.

• According to data from the Framingham study, cholesterol levels made no difference in cardiovascular mortality for men above age 47.

• A study at Yale found that nearly twice as many people with low cholesterol had heart attacks when compared to those with high cholesterol levels.

• Statins stimulate cancer growth in rodents.

• Human studies found that breast cancer was more common in women who took statins than in the control group.

• A study in the Netherlands found that men with low cholesterol levels had an increased risk of depression.

• A study found that simvastatin increases insulin levels by 13 percent, increasing the risk of heart disease, hypertension, obesity, insulin resistance, and Type 2 diabetes.

• Studies find that people taking calcium channel blockers actually experience a 60 percent increase in heart attack compared to people who used other blood pressure medications.

• A study found that patients taking amlodipine had a 38 percent higher risk of heart failure.

• A study showed that 96 percent of articles in medical journals that supported the use of calcium channel blockers were written by doctors with financial ties to the drug maker.

• A study in Japan found that subjects who took nitrates on a regular basis were 2.4 times more likely to have a major cardiac event than those who didn’t take the drugs.

• In one study of people who had had a stroke but had no other risk factors, 90 percent had elevated homocysteine.

• The Physician’s Health Study concluded that participants with high homocysteine levels are three times more likely to have a heart attack.

• A study found that once C-reactive protein levels reached twice the normal level, study participants were 150 percent moe likely to suffer a heart attack.

• A study found that men with the highest levels of C-reactive protein were twice as likely to have had a stroke and three times as likely to have had a heart attack as the men with normal CRP levels.

• Research at Harvard Medical School found that women with the highest levels of C-reactive protein were at 4.4 times the risk of heart attack as women with the lowest levels.

• A study found that a person eating 4 ounces of sugar daily is five times more likely to have a heart attack than someone who eats 2 ounces of sugar daily.

• Starch transforms into acrylamide (a carcinogen) when heated.

• A study at Johns Hopkins found that mercury levels were 15 percent higher in men who had heart attacks.

• A study found that vegans had homocysteine levels 50 percent higher than omnivores.

• A study found that men drinking milk gained more muscle than men who drank a carbohydrate drink.

• A 17-year study of over 21,000 men found that nut eaters are 50 percent less likely to die from heart rhythm problems and 30 percent less likely to die from heart disease than non-nut eaters are.

• A study found that protein helps the body absorb calcium, which in turn negates the adverse effects protein may have on calcium loss from the bones.

• A study in the Netherlands found that trans fatty acid intake is directly associated with an increased risk of coronary heart disease.

• The Physician’s Health Study found that men who consume alcohol daily have a 40 percent decrease in the risk of cardiovascular disease, but men who drink more than two drinks a day have a higher risk of death.

• A 12-year study of 47,000 men from age 40 to 75 found that men who drink 1.5 drinks a day have a 36 percent lower risk of developing diabetes.

• Supplemental carnosine helps prevent glycation.

• A study found that subjects who ate a low-starch diet weight markedly less than those who ate a high-starch diet.

• A study found that high-protein diets increase a substance called PAI-1 in the blood, which inhibits the production of fat.

• A study found low levels of coenzyme Q10 in 50 to 75 percent of patients with various types of heart disease.

• A study found that 43 percent of patients taking coenzyme Q10 were able to cut back or eliminate their cardiac medication.

• A study of patients with high blood pressure found that 51 percent of subjects were able to discontinue their blood pressure medication after taking coenzyme Q10 supplements.

• A study found that patients with angina pectoris experienced a 53 percent reduction in the frequency of their angina attacks after taking coenzyme Q10.

• A study of heart tissue found that old heart tissue pre-treated with coenzyme Q10 recovered 72 percent of its contraction after being deprived of oxygen and glucose.

• A study of animals who were poisoned to bring on a physical state similar to that caused by Huntington’s disease or ALS found that the animals receiving supplemental coenzyme Q10 experienced much less damage caused by the poison.

• Researchers found that people suffering from cancer had lower levels of coenzyme Q10 in the blood than people without cancer did.

• A study of patients with Parkinson’s disease found that those taking the highest doses of coenzyme Q10 had a 44% less decline in normal daily functions.

• Carnitine reduces arterial plaque, lowers LDL cholesterol, and increases HDL levels.

• A study found that men taking L-arginine while participating in a strength training program showed a significantly greater increase in muscle strength and lean muscle mass after only five weeks.

• Studies of over 100,000 health workers found that those who took daily vitamin E supplements for a minimum of two years had about a 40 percent lower risk of developing heart disease, a 29 percent lower risk of stroke, and a 13 percent reduction in overall death rates.

• Mixed tocopherol supplementation increases the elasticity of the arteries, increases blood circulation, and decreases the stickiness of platelets.

• A study found a dramatic decline in death from heart disease among men with the highest vitamin C intake.

• A study showed that a glutamine cocktail helped people with cancer reverse their muscle loss.

• A study that measured the concentrations of lycopene in fat tissue found that people with higher tissue lycopene levels experienced lower risks of heart attack.

• Omega-3 fatty acids can calm irregular heart rhythms, lower blood pressure, and lower triglycerides.

• A Harvard study found that the more men eat foods rich in omega-3 fatty acids, the lower their risk of stroke.

• A study by the US Department of Veterans Affairs found that men with severe periodontal bone loss had 150 percent greater risk of heart disease.

• Studies find that garlic lowers systolic blood pressure by 20 to 30 mm Hg and diastolic by 10 to 20 mm Hg.

• Hawthorn lowers blood pressure, improves coronary circulation, prevents cholesterol deposits from forming on artery walls, and helps strengthen the heart muscle.

• A study found that hawthorn reduced anxiety better than magnesium or a placebo.

• 96 percent of patients in a recent study were able to reduce their need for type 2 diabetes medicine after eating almonds.

• People with adult-onset diabetes can lower their insulin requirements by taking chromium.

• A study of patients with diabetes found that only 17 of those taking a multivitamin developed an infection, while 93 percent of those taking the placebo became sick.

• In one study, 23 percent of patients with type 2 diabetes were able to discontinue their oral insulin when taking gymnema sylvestre. All patients in the study were able to reduce their insulin dosage.

• Elderly participants who took part in a resistance-training program for 11 weeks increased their muscle mass by up to 60 percent.

• An analysis of 684 identical twins found that the twin who exercised regularly had a significantly lower risk of developing heart disease than the twin who did not exercise.

The Language of Life is a book by Dr. Francis Collins, a physician and geneticist who is Director of the National Institutes of Health. This post has some notes from the book.

• Family health history is the strongest of all currently measurable risk factors for many common conditions.

• A mutation in the HERG gene is involved in long QT syndrome. Individuals with mutations linked to long QT syndrome can have their risk greatly reduced by lifelong treatment with beta-blockers.

• Women who carry a BRCA1 mutation have about an 80 percent lifetime riks of developing breast cancer and a 50 percent risk of developing ovarian cancer.

• VX-770 reduces the sweat chloride levels for treated individuals with cystic fibrosis to nearly normal.

• The March of Dimes currently recommends screening newborns for 29 conditions.

• A mutation in the LRRK2 gene can confer a high risk of Parkinson’s disease.

• Almost 80 percent of the risk for macular degeneration can be inferred from two genetic risk factors, combined with just two environmental risk factors (smoking and obesity).

• Individuals with rheumatoid arthritis, who receive high doses of anti-inflammatory agents to try to control their arthritis, have a very low incidence of macular degeneration.

• Variations in a single gene have been implicated in type 1 diabetes, rheumatoid arthritis, and Crohn’s disease.

• There are three major factors that people generally use to assess whether or not they want genetic risk information:

1. How big is the risk (in terms of the absolute risk)?

2. What is the burden of the disease?

3. What can I do about it?

• The Cancer Genome Atlas catalogs mutations associated with cancers.

• In a trial in Japan for patients with lung cancer who had proven mutations in the EGFR gene, 63 percent of patients responded quite positively to gefitinib.

• The DNA sequence of any two individuals is 99.6 percent identical, regardless of which parts of the world their ancestors came from.

• Only about 1 percent of Europeans have the complete loss of the protein CCR5, but these individuals are essentially protected from infection with most strains of HIV.

• A stem cell transplant from a person with a mutation in the CCR5 gene was able to eliminate HIV in an infected patient.

• Individuals who lack the G6PD enzyme in their red blood cells do better after exposure to malaria.

• Variations in SLC11A1 and TLR2 are involved in susceptibility to tuberculosis.

• Each child of an individual with Huntington’s disease has a 50 percent chance of inheriting the genetic mutation and developing the disease.

• The identical twin concordance is 50 percent for schizophrenia, 60 percent for bipolar disorder, 40 percent for major depressive disorder, and as high as 90 percent for autism.

• A study of males in New Zealand revealed that the variant associated with lower MAOA activity was associated with violent behavior and criminal convictions.

• Researchers studied more than same-sex twin pairs and their spouses in Sweden and identified a variant in the V1aR gene showing statistically significant association with a variety of measures of marital satisfaction or stress. Males carrying two copies of the “risk” variant reported a 34 percent incidence of marital crisis or threat of divorce in the previous year, whereas those carrying no copies of the risk allele reported only 15 percent.

• Performance on an IQ test reflects approximately 50 percent heredity and approximately 50 percent nonheritable factors.

• Studies of families and identical twins reveal that roughly 70 percent of the risk of late-onset Alzheimer’s disease is genetic.

• A person carrying two copies of the e4 allele of APOE has an eightfold increased risk of Alzheimer’s disease.

• Farnesyl transferase inhibitors may prevent and treat cardiovascular disease in children with progeria. The class of medication may also extend lifespan.

• The condition of the enzyme CYP2C19 may explain the variation in the response to clopidogrel.

• 29,000 visits to emergency rooms each year are attributed to coumadin overdoses.

• Variations in the genes CYP2C9 and VKORC1 can account for about 40 percent of the variability in the therapeutic dose of coumadin.

• Avoiding the use of abacavir in patients who are HLA-B*5701-positive almost completely eliminates the hypersensitivity reaction.

• Those who carry one copy of a common variant in the SLC01B1 gene have a fourfold increase in the risk of muscle toxicity from statins. Those who carry two copies of the variant increase that risk by a factor of 16.

• Gene therapy treatments for patients with Leber’s congenital amaurosis show great promise.

• Recent experiments on rats have shown that stem cells can encourage reconnection of the transected spinal cord.

The Paleo Diet is a book by Dr. Loren Cordain, a professor at Colorado State University. The book was originally published in 2001 and has been updated in a revised edition. This post has notes on some of the scientific studies mentioned in the revised edition of the book.

• Research at the Royal Melbourne Institute of Technology found that acne patients reported significant improvements on a high protein low-glycemic-load diet.

• Studies of Greenland Eskimos showed that despite a diet containing more than 60 percent animal food, not one death from heart disease – or even a single heart attack – occurred in 2,6000 Eskimos from 1968 to 1978.

• In Paleolithic times, the main saturated fat in wild animals was healthful stearic acid.

• Chronic low-level inflammation triggers the rupture of the fibrous cap that surrounds plaque that forms in the heart’s arteries, which then causes a clot to form and results in a heart attack.

• A study of the bone mineral status of elderly men and women found that the people who ate the most fruits and vegetables had the greatest bone mineral density and the strongest bones. More than 100 scientific studies have confirmed this.

• A study showed that taking potassium bicarbonate neutralized the body’s internal acid production, reduced urinary calcium losses, and increased the rate of bone formation.

• Studies show that high-protein diets are more effective than low-fat, high-carbohydrate diets in lowering triglycerides.

• A study showed that people who eat a lot of lean meat have lower blood levels of homocysteine (a toxic substance in the blood that damages the arteries and predisposes them to atherosclerosis) than do vegan vegetarians.

• A study of sixty-five overweight people on a high-protein diet for six months found that their kidneys easily adapted to increased protein levels.

• Hundreds of studies have demonstrated that high-protein, low-calorie diets are much more effective than low-calorie, high-carbohydrate diets.

• Having a low magnesium level puts people at risk for heart disease by elevating blood pressure and predisposing the heart to irregular beats. A low intake of magnesium also promotes the formation of kidney stones.

• A series of studies found that the bones of Paleolithic people who lived in England 12,000 years ago indicated that their diet was almost identical to that of top-level carnivores, such as wolves and bears.

• We can only tolerate about 200 to 300 grams of protein per day. Too much protein can lead to nausea, diarrhea, and even death.

• Studies of the bones of early farmers found that they had more infectious diseases than their ancestors, more childhood mortality, and shorter life spans in general. They also had more osteoporosis, rickets, and other bone mineral disorders.

• Cereal grains and legumes contain antinutrients that can prevent the body from absorbing the proper nutrients and damage the gastrointestinal and immune systems.

• Research shows that fructose can cause insulin resistance in humans, which in turn promotes obesity and chronic metabolic syndrome diseases, including hypertension, heart disease, and diabetes.

• The ratio of omega 6 to omega 3 fats in Paleo diets was about 2 to 1. Eating too many omega 6 fats instead of omega 3 fats increase the risk of heart disease and certain forms of cancer. It also aggravates inflammatory and autoimmune diseases.

• A study found that consumption of trans fats was responsible for more than 30,000 deaths annually from heart disease.

• A study of vegetarian women from Nepal found low levels of vitamin B6 resulting from high levels of pyridoxine glucosides in their diets.

• Experiments show that wheat and other whole grains impair the body’s ability to get enough biotin, which is important for the health of nails and hair.

• Low dietary intake of vitamin B6, vitamin B12, and folate increases the blood level of homocysteine, which in turn increases the risk of heart disease.

• Studies have found that flatbread consumption in the Middle East causes a zinc deficiency that stunts growth and delays puberty in children.

• Research found that during a twenty-four-hour period, a high-protein diet increased total energy expenditures by 12 percent compared to a calorically matched high-carbohydrate diet.

• Research found that high-protein meals are much more effective than high-fat meals in satisfying the appetite.

• A study found that after twenty-one days on a high-protein diet, a group of women had significantly improved insulin metabolism, but those on a high-carbohydrate diet got worse.

• A study in Denmark found that the average weight loss on a high-protein diet was 19.6 pounds after six months, whereas a high-carbohydrate group lost only an average of 11.2 pounds.

• A study found that women on a higher-protein diet had higher levels of thyroid hormone, which indicates that they had a faster metabolic rate. The higher protein diet also resulted in a noticeable drop in triglyceride levels.

• Multiple scientific studies have shown that there is a strong association between elevated levels of IGF-1, lowered levels of IGFBP-3, and breast cancer in premenopausal women, prostate cancer in men, and colorectal cancer in all adults. In animal models of many types of cancer, scientists can promote cancer by adding IGF-1. They can slow the growth of cancer by adding IGFBP-3.

• Grain-based and starch-based diets increase the risk of breast cancer because they elevate insulin – which in turn increases IGF-1 and lowers IGFBP-3.

• Elevated insulin contributes to the excessive growth of the eyeball which leads to myopia.

• Eating foods that can improve insulin metabolism can reduce many of the symptoms of polycystic ovary syndrome.

• A study of Inuit natives found that when they ate their traditional foods, acne was absent. When they adopted Western foods, acne appeared.

• Broccoli contains substances that fight cancer.

• Strawberries, tomatoes, pineapples, and green peppers contain p-coumaric acid and chlorogenic acid, compounds which are anticancer agents.

• Garlic and onions are sources of allylic sulfides, which seem to protect against stomach cancer.

• Studies in humans and animals have shown that salt can constrict the muscle surrounding the small airways in the lung.

• Fish oil capsules can reduce the inflammation of Crohn’s disease and ulcerative colitis.

• Research groups have shown that milk, grain, legume, and nightshade proteins can trick the immune system into attacking the body’s own tissues.

• Research by Dr. Klaus Lorenz found that populations eating little or no wheat, rye, or barley have very low rates of schizophrenia.

• Research by Dr. F. Curtis Dohan found that the symptoms of schizophrenia were reduced in patients on grain-free and dairy-free diets but worsened when those foods were returned to the diet.

• Research by Dr. Joe Hibbeln has demonstrated that omega 3 fats may be effective in reducing symptoms of depression, hostility, schizophrenia, and other mental disorders.

• Research involving patients with bipolar disorder found that a group taking omega 3 fatty acids performed better than the placebo group on nearly every outcome measure.

• Studies have shown that people with high lifetime sunlight exposure have lower rates of melanoma than those with low sunlight exposure.

• Evidence from population studies shows that people with the greatest lifetime sun exposures have the lowest rates of prostate, breast, and colon cancers.

• Studies of laboratory animals have found that excessive omega 6 fats promote the development of skin cancer – but omega 3 fats slow it down.

• Almost all nuts have high levels of omega 6 fats, and if eaten excessively, they can unbalance the ratio of omega 6 to omega 3 in the diet.

• Numerous scientific studies have demonstrated the omega 3 fatty acid inferiority of farmed fish compared to wild fish.

• The canning process increases the level of oxidized cholesterol in fish, specifically 25-hydroxycholesterol that is extremely destructive to the linings of arterial blood vessels.

• High heat produces more oxidized cholesterol than slow cooking.

• A series of rat studies of canola oil reported kidney injuries, behavioral changes, and liver injuries.

• Peanut oil is routinely used to induce coronary artery atherosclerosis in monkeys and other laboratory levels.

• The lauric acid found in coconut oil exerts a protective effect by eliminating gut bacteria that increase intestinal permeability, a risk factor for cardiovascular disease via heightened chronic low-level inflammation.

• Studies have shown that capsaicin increases intestinal permeability and may play a role in the development and progression of certain autoimmune diseases.

• Daily supplementation of 500 to 1,000 milligrams of vitamin C has been shown to improve immune function and lower the risk of certain types of cancer.

• A study of selenium found that doses of 200 micrograms reduced the overall incidence of cancer by 42 percent and cut cancer death rates in half.

• A review of long-term randomized trials found that weight losses were greater in people who combined diet and exercise, compared to people who only dieted.

• Regular exercise improves the muscles’ sensitivity to insulin and lowers the level of insulin in the bloodstream.

• Exercise has been shown to lower the triglyceride level (which may be a risk factor for atherosclerosis and coronary heart disease).

• Regular physical exertion has been shown to widen and increase the elasticity of the coronary arteries that carry blood to the heart.

• Studies have demonstrated that exercise is effective in lowering blood pressure.

Relaxation Revolution is a book written by Harvard Medical school professor Dr. Herbert Benson with Harvard law graduate William Proctor. Dr. Benson has studied mind body medicine and the relaxation response for decades. The book summarizes some of this research. This post has some notes from the scientific research discussed in the book.

Phase One: Relaxation Response Trigger

1. Pick a focus word, phrase, image, or short prayer. Or focus only on your breathing during the exercise.

2. Find a quiet place and sit calmly in a comfortable position.

3. Close your eyes.

4. Progressively relax all your muscles.

5. Breathe slowly and naturally. As you exhale, repeat or picture silently your focus word or phrase, or simply focus on your breathing rhythm.

6. Assume a passive attitude. When other thoughts intrude, simply think, “Oh well,” and return to your focus.

7. Continue with this exercise for an average of 12 to 15 minutes.

8. Practice this technique at least once daily.

Phase Two: Visualization

Use mental imagery, such as picturing a peaceful scene in which you are free of your medical condition, to engage healing expectation belief, and memory. This second phase will usually require an average of 8 to 10 minutes.

Notes:

• When specific signatures of gene expression were examined before and after relaxation response training, 1,561 genes changed expression from the first test to the second.

• Gene signatures that were switched on or off in a group of novice meditators and a group of experienced meditators were associated through past research with clear health benefits.

• A study showed that relaxation response training leads to an increase of nitric oxide throughout the body. Nitric oxide can protect the body from microbes, cardiovascular disorders such as hypertension, and immune problems.

• An fMRI study showed that people who were experienced in eliciting the relaxation response through meditation had thicker regions of the brain’s cortex in decision-making regions associated with attention and also sensory, cognitive, and emotional processing. The greater cortical thickness in older participants’ brains suggests that meditation might offset age-related cortical thinning.

• A study found that relaxation response patients with high blood pressure were much more likely than a control group to be successful in eliminating their use of an antihypertensive medication.

• Research combining stimulus control, the relaxation response, and various behavioral techniques enabled 91 percent of insomnia patients to either eliminate or reduce their drug use. All of the participants reported improved sleep after the study, with the majority (58 percent) reporting significant improvement.

• A study of patients who were on medication for irregular heartbeats found that relaxation response training led to a reduced frequency of PVCs in 8 of the 11 patients.

• In women with the most severe PMS symptoms, the relaxation response showed a 58 percent improvement, compared to a 17 percent improvement for the control group.

• A study of women who had been infertile for an average of 3.3 years found that a program of meditation and stress management led to 34 percent of the women becoming pregnant within six months of completing the program.

• A study using fMRI found that the relaxation response led to beneficial changes in the attention and executive control parts of the subjects’ brains.

• An analysis of 27 studies on patients recovering from a heart attack found that when patients were given at least nine hours of supervised instruction of relaxation therapy, several benefits ensued: The frequency of angina pectoris was reduced, irregular heartbeats and exercise-induced ischemia were reduced, and work attendance improved. Also, cardiac events occurred less frequently, and there were fewer cardiac deaths.

• Studies of mind body treatments have found that pounding heartbeats (palpitations) decline from a rate of once or twice a month to less than once a month. Shortness of breath also decreases noticeably as a result of mind body treatments.

• A study of 150 women with breast cancer who experienced hot flashes found that the incidence, severity, and distress caused by hot flashes declined significantly over a one-month period in the relaxation group in comparison with the control group.

• A study found that nausea symptoms decreased dramatically in frequency after patients learned to elicit the relaxation response.

• A study of breast cancer patients found that progressive muscle relaxation training considerably decreased the duration of nausea and vomiting.

• Studies by Margaret Caudill have demonstrated that the relaxation response can be powerful anti-pain treatment.

• Studies show that about 60 percent of patients with migraine headaches experience fewer and less severe headaches after they use relaxation response techniques.

• A mind body intervention study found a 36 percent reduction in clinic visits in neck and shoulder pain patients who received relaxation response training.

• A study of cardiac surgery patients found that those who practiced the relaxation response technique had a lower incidence of postoperative rapid heartbeats (supraventicular tachycardia) than did the control group. They also experienced greater decreases in psychological tension.

• A study of rectal and anal surgery patients found that relaxation training and guided imagery led to a significant improvement in the quality of sleep and a decrease in anxiety.

• Studies show that the relaxation response triggers physiologic reactions that are associated with altered autonomic nervous system activity – changes in the body that help counter the anxiety symptoms associated with a phobic reaction.

• A study of patients with fear of blood who received applied relaxation training showed that 73 percent of the patients had improved clinically at the end of the treatments.

• A study of patients with an average age of 71.3 years found that the relaxation response-trained group achieved significant improvement on a simple task requiring basic mental and motor skills.

• A study found that the gene set expression in long-term relaxation response practitioners was counter to the gene expression in various cancers: lymphoma (follicular and B cell lymphoma), neuro tumors (central nervous system and glioma), liver, leukemia (myeloid, acute promyelocytic, B cell chronic leukemia), multiple myeloma, B cell chronic lymphoblastic leukemia, and another form of leukemia.

• The results of a study of long-term relaxation response practitioners showed gene set expression that was consistent with the expression found in certain anticancer therapies.

• A study of short-term meditation trainees found that after eight weeks, their gene set expression signatures countered or opposed the gene signatures for such cancers as neuro tumors, multiple myeloma, and leukemia.

• A study of students at the Horace Mann Middle School in South Central Los Angeles found that those who had attended more than two semester-long relaxation response classes had higher grade point averages, better work habits, and higher levels of cooperation than did students who attended two or fewer such classes.

Inflammation Nation is a book written by Dr. Floyd Chilton, a professor at Wake Forest University. In the book, he discusses the role of inflammation in many diseases and describes a plan to reduce inflammation. This post has some notes on the scientific research discussed in the book. Gene Smart Wellness offers an omega 3 home blood test kit for individuals to check their level of inflammation.

• Inflammatory diseases affect as many as half of the people in the USA.

• Normal weight people have adiponectin circulating at a relatively high concentration in the blood. Those levels drop precipitously in overweight people. Adiponectin has anti-inflammatory properties, such as inhibiting the production of pro-inflammatory messengers like TNF-alpha.

• The evidence that atherosclerosis is an inflammatory disease has been significantly bolstered by studies that show the predictive power of a marker of inflammation called C-reactive protein.

• People who have taken anti-inflammatory drugs for a long period of time to treat another condition, like arthritis, have a reduced risk of contracting Alzheimer’s.

• Chronic inflammation predisposes humans to carcinoma [cancer] in the breast, liver, large bowel, urinary bladder, prostate, gastric mucosa, ovary, and skin.

• The use of anti-inflammatory drugs reduces colon cancer risk by 40 to 50 percent and also may be preventive for lung, esophagus, and stomach cancer.

• A study of the Chilton Program found that leukotriene production was suppressed in 78 percent of the asthma sufferers in the study.

• Clinical trials in humans have found that the more dietary arachidonic acid humans consume in foods, the more inflammatory messengers they produce.

• A study showed that people on a high-AA diet (1,500 mg a day) had 41 percent more of the messengers that control inflammation and platelet stickiness than people on a low-AA diet (210 mg a day).

• The concentration of AA in the blood increases as people age.

• A four-ounce portion of farmed Atlantic salmon – less than the size of a standard filet – contains 1,307 mg of AA. That’s more than thirteen times the amount of daily AA that’s recommended in the Chilton Solution diet.

• One study introduced very high levels of arachidonic acid into the diets of four study participants for twenty-one days. After just two weeks, the participants had dramatic increases in irreversible platelet aggregation, a leading contributor to heart attack.

• While a four-ounce portion of farmed Atlantic salmon contains 1,306 mg of AA, a piece of wild Atlantic salmon the same size has only 303 mg of AA. The same portion of wild Chinook salmon has only 175 mg of AA.

• Eggs are one of the most significant sources of AA in our diets, with very little of the beneficial fatty acids to correct the balance.

• In almost all animals, organ tissues have higher amounts of AA than other tissues.

• Beef and lamb are comparatively low in AA (as long as you stay away from organ tissues), and beef fat actually contains slightly less AA than the lean meat does. Lean beef and lamb contain higher levels of beneficial omega-3 fatty acids than white meats, which are high in AA.

• EPA and DGLA work in tandem to act as inflammation fighters, by helping to block the production of inflammatory messengers from AA, as well as another category of inflammatory messengers called cytokines.

• A study of stearidonic acid found in Echium plantagineum showed that around 70 percent of people in the study responded to the planet oil and had a 30 percent reduction in triglycerides.

• When people ingest gammalinolenic acid, inflammatory cells will take it up and rapidly convert it into DGLA. This leads to the accumulation of a natural – and very powerful – inhibitor of enzymes that convert AA to inflammatory messengers.

• Borage seed is an ideal source of GLA, because more than 20 percent of the fatty acids in the seed oil is GLA.

• A placebo-controlled trial found that high doses of GLA caused market reductions in the number of, and in the pain from, tender joints in patients with rheumatoid arthritis.

• At least 600 mg of GLA are required each day to have significant effects on the inflammatory messengers produced by our body.

• The conversion of GLA to AA by the liver can easily be blocked by increasing consumption of eicosapentaenoic acid (EPA). If you are taking high levels of anti-inflammatory GLA, you must make sure you are getting enough EPA to block the potentially dangerous side effect of this powerful supplement.

• High levels of glucose and insulin that result from refined carbohydrate consumption are linked to the production of inflammatory messengers from AA.

• Six clinical trials reveal that the fatty-acid balance in the Chilton Program blocks the production of inflammatory messengers that cause signs and symptoms of inflammatory diseases.

• In asthmatics, it took just seven to ten days of supplementation with the right amounts of ratios of GLA and EPA to see significant effects on the inflammatory messengers that cause the signs and symptoms of asthma.