Daniel Amen
Dr. Daniel Amen is a researcher and author working in the field of neuroimaging and psychiatric health. His published research focuses primarily on using brain single-photon emission computed tomography (SPECT) imaging to assess regional cerebral blood flow and neural connectivity. His work investigates functional brain imaging biomarkers across psychiatric and neurological conditions, including major depressive disorder, schizophrenia, ADHD, cognitive disorders, and the effects of adverse childhood experiences.
17 claims checked on air: 2 context 1 contradicted 12 supported 2 unverified
What they said on air
4 citing their own research
Social isolation is a risk factor for dementia.
"isolation is actually a risk factor for dementia" (said at 0:17:09)
Large-scale systematic reviews, meta-analyses, and umbrella reviews of prospective longitudinal cohort studies confirm that social isolation (along with loneliness and low social engagement) is an established modifiable risk factor for incident dementia, associated with an approximately 1.5-fold increased risk of developing the condition.
- supports: COVID-19, loneliness, social isolation and risk of dementia in older people: a systematic … (International journal of psychiatry in clinical practice 2022) · cited 111x in the literature
"Results of the meta-analysis show that in older people, the risk of developing dementia because of the impact of prolonged loneliness and social isolation is about 49 to 60% [HR/HR = 1.49; CI 95 =1.37-1.61] higher than in those who are not lonely and socially isolated." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Potentially Modifiable Risk Factors for Dementia and Mild Cognitive Impairment: An Umbrell… (Dementia and geriatric cognitive disorders 2024) · cited 90x in the literature
"We identified fourteen broadly defined modifiable risk factors that were significantly associated with these disorders: alcohol consumption, body weight, depression, diabetes mellitus, diet, hypertension, less education, physical inactivity, sensory loss, sleep disturbance, smoking, social isolation, traumatic brain injury, and vitamin D deficiency. All 14 factors were associated with the risk of major NCD" (abstract, results, passage verified)
pubmedfull study (doi)
Social isolation is a trigger for depression.
"it's clearly a trigger for depression." (said at 0:17:13)
Extensive epidemiological and longitudinal evidence supports the claim that social isolation (and the related experience of loneliness) is a significant risk factor and precipitating trigger for the onset of depressive symptoms and major depression. A meta-analysis examining social isolation in older adults (PMID: 41578462) identified a 60% increased likelihood of depressive symptoms (pooled OR = 1.60, 95% CI: 1.39–1.84). Similarly, a systematic review and meta-analysis of prospective cohort studies (PMID: 35583561) evaluating the new onset of mental health disorders found that baseline social disconnection/loneliness more than doubled the adjusted risk of subsequent incident depression (pooled adjusted OR = 2.33, 95% CI: 1.62–3.34).
A breathing pattern of 3-4 seconds inhalation and 6-8 seconds exhalation triggers a parasympathetic nervous system response.
"we had worked on this very specific breathing pattern. It's been found to trigger a parasympathetic response, which is basically three or four seconds in, so take a deep breath, and then six to eight seconds out." (said at 0:21:56)
Paced slow breathing with prolonged exhalation (typically a 1:2 inhalation-to-exhalation ratio, such as 3-4 seconds inhaling and 6-8 seconds exhaling, corresponding to roughly 6 breaths per minute) is well-documented to enhance vagally mediated heart rate variability (HRV) and activate parasympathetic nervous system activity. Experimental studies and randomized trials demonstrate that prolonging the exhalation phase relative to inhalation increases high-frequency heart rate variability (HF-HRV) and the root mean square of successive differences (RMSSD), established physiological markers of cardiac vagal tone.
Dr. Amen scanned and evaluated 300 NFL players in a study starting in 2009 and found high levels of brain damage.
"I did the big NFL study starting in 2009. We scanned and treated 300 NFL players: high levels of damage." (said at 0:24:15)
Dr. Amen and colleagues initiated an ongoing longitudinal study in 2009 evaluating active and retired NFL players using SPECT perfusion neuroimaging and clinical evaluations. Published findings from this cohort reported significant hypoperfusion across 36 brain regions consistent with traumatic brain injury in 161 NFL players compared to 124 healthy controls, and a pilot open-label intervention study evaluated and treated 30 players. The certainty is low due to observational and open-label study designs.
Dr. David Smith founded the Haight Ashbury Free Clinic.
"David Smith, who's founder of the Haight Ashbury Free Clinic and really thought of as the father of addiction medicine in the United States" (said at 0:29:10)
Historical records and scholarly literature document that Dr. David E. Smith founded the Haight Ashbury Free Medical Clinic (HAFMC) in San Francisco in 1967. The clinic was established during the counterculture movement to provide free, nonjudgmental healthcare and addiction treatment to underserved populations, cementing Smith's role as a pioneer in the development of modern addiction medicine.
Brain damage from head trauma increases the risk of addictive behavior and loss of behavioral control.
"You damage your brain, you're more likely to have behavior that gets out of control." (said at 0:29:45)
Traumatic brain injury (TBI) is well-documented in clinical neurotrauma and psychiatric literature to elevate the risk of behavioral dyscontrol, impulsivity, disinhibition, aggression, and addictive behaviors (such as substance use disorders and problem gambling). Systematic reviews and meta-analyses estimate that substantial proportions of TBI patients develop post-injury personality changes characterized by poor impulse control, emotional lability, and behavioral disinhibition.
- supports: Agitation, aggression, and disinhibition syndromes after traumatic brain injury. (NeuroRehabilitation 2002) · cited 146x in the literature
"Traumatic brain injury (TBI) is frequently complicated by disinhibition and aggression. These often profound changes in personality, present obstacles to rehabilitative treatments and community reentry. Syndromal presentations may involve a loss of impulse control, spontaneous aggression, and dysphoric bipolar states." (abstract, results, passage verified)
pubmed - supports: Moderate to severe gambling problems and traumatic brain injury: A population-based study. (Psychiatry research 2019) · cited 19x in the literature
"Traumatic brain injury (TBI) is a common injury characterized by a change in brain function after an external blow to the head and is associated with substance abuse, psychological distress, risk-taking, and impulsivity." (abstract, background, passage verified)
pubmedfull study (doi) - supports: Personality change after traumatic brain injury: a systematic review and meta-analysis. (Journal of neurology 2026)
"Personality change was defined inconsistently although common symptoms involved the emergence or increase of affective, behavioral, and social disturbances, including irritability, depression, emotional instability, anger outbursts, social withdrawal, anxiety, impulsivity, restlessness, aberrant motor behaviors, and aggression. The prevalence of secondary personality disorder was estimated as 29.1% (CIs 22.5% - 36.2%) and prevalence of broad personality change was 68.1% (CIs 53.4% - 81.2%)." (abstract, results, passage verified)
pubmedfull study (doi)
Frequent massive dopamine surges lead to desensitization in the nucleus accumbens, requiring higher stimulation to experience pleasure.
"dopamine is really important and it presses on the nucleus accumbens, but if you dump it, it presses too hard, just like fame. So think of Miley or Justin. They get all of this dopamine, well, it wears it out, and then they need more and more in order to feel anything at all." (said at 0:30:00)
Extensive neuroimaging and preclinical research supports the concept that repeated, supraphysiological dopamine release in the reward circuitry (including the nucleus accumbens) leads to neuroadaptive down-regulation. Human positron emission tomography (PET) studies demonstrate that chronic excessive stimulation blunts striatal dopamine release and decreases dopamine D2 receptor availability in the nucleus accumbens and dorsal striatum. These neuroadaptations reduce baseline sensitivity to everyday rewards and require increasingly potent stimuli to achieve equivalent dopamine signaling and subjective reward.
- supports: Addiction: beyond dopamine reward circuitry. (Proceedings of the National Academy of Sciences of the United States of America 2011) · cited 958x in the literature
"These studies have corroborated in humans the relevance of drug-induced fast DA increases in striatum [including nucleus accumbens (NAc)] in their rewarding effects but have unexpectedly shown that in addicted subjects, drug-induced DA increases (as well as their subjective reinforcing effects) are markedly blunted compared with controls... Also, whether tested during early or protracted withdrawal, addicted subjects show lower levels of D2 receptors in striatum (including NAc)..." (abstract, passage verified)
pubmedfull study (doi) - supports: The Brain on Drugs: From Reward to Addiction. (Cell 2015) · cited 1311x in the literature
"Drugs of abuse exert their initial reinforcing effects by triggering supraphysiologic surges of dopamine in the nucleus accumbens that activate the direct striatal pathway via D1 receptors and inhibit the indirect striato-cortical pathway via D2 receptors. Repeated drug administration triggers neuroplastic changes in glutamatergic inputs to the striatum and midbrain dopamine neurons, enhancing the brain's reactivity to drug cues, reducing the sensitivity to non-drug rewards, weakening self-regulation, and increasing the sensitivity to stressful stimuli and dysphoria." (abstract, passage verified)
pubmedfull study (doi)
Dopamine acts directly on the nucleus accumbens in the brain.
"So dopamine is really important and it presses on the nucleus accumbens, but if you dump it, it presses too hard, just like fame." (said at 0:30:27)
The mesolimbic dopaminergic pathway is a well-established neural circuit in which dopamine-producing neurons projecting from the ventral tegmental area directly innervate the nucleus accumbens. Dopamine released into the nucleus accumbens binds to local dopamine receptors (such as D1 and D2 receptors) to regulate intracellular signaling, synaptic plasticity, reward processing, and motivated behavior.
- supports: Nucleus Accumbens as a Novel Target for Deep Brain Stimulation in the Treatment of Addicti… (Neurology India 2019) · cited 18x in the literature
"The three stages of the addiction cycle are known to be mediated by dopaminergic pathways located in the mesolimbic dopamine system with connections to dorsal striatum, extended amygdala, cingulate gyrus, orbitofrontal cortex, prefrontal cortex, and ventral tegmental area. Recent advanced neuroimaging in humans and several animal studies demonstrated NA to be a vital anatomical area modulating this network." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Phosphorylation Signals Downstream of Dopamine Receptors in Emotional Behaviors: Associati… (International journal of molecular sciences 2022) · cited 13x in the literature
"Dopamine regulates emotional behaviors, including rewarding and aversive behaviors, through the mesolimbic dopaminergic pathway, which projects dopamine neurons from the ventral tegmental area to the nucleus accumbens (NAc)." (abstract, background, passage verified)
pubmedfull study (doi)
Tom Brady gets nine hours of sleep per night and avoids gluten, dairy, corn, soy, artificial dyes, sweeteners, and sugar.
"Gets nine hours of sleep, he doesn't eat gluten, dairy, corn, soy, artificial dyes, sweeteners, sugar. I mean, his diet is really clean" (said at 0:50:20)
No published record matching the specific daily sleep duration and dietary exclusions of Tom Brady was located in the scientific literature; this does not prove the claim false. While the described nutritional rules align broadly with public descriptions of the commercial "TB12 Method" lifestyle program, individual lifestyle regimens of specific athletes are not documented or evaluated in peer-reviewed biomedical research.
Chronically high blood sugar damages blood vessels, causing them to lose flexibility and become brittle and prone to breaking.
"Which is an emergency, because when your blood sugar is chronically high, it erodes your blood vessels, making them more likely to lose their flexibility, be brittle, and more likely to break." (said at 0:55:35)
Published literature confirms that chronic hyperglycemia drives vascular damage through multiple well-characterized pathways, including endothelial dysfunction, oxidative stress, advanced glycation end-product (AGE) cross-linking of extracellular matrix proteins, and vascular smooth muscle calcification. These pathophysiological alterations directly result in loss of arterial compliance (increased arterial stiffness) and structural vessel wall fragility, which predisposes to microvascular and macrovascular injury.
- supports: Mechanisms, significance and treatment of vascular dysfunction in type 2 diabetes mellitus… (Drugs 2005) · cited 84x in the literature
"Hyperglycaemia also contributes to accelerated arterial stiffening by increasing formation of advanced glycation end-products (AGEs), which alter vessel wall structure and function." (abstract, results, passage verified)
pubmedfull study (doi) - supports: Arterial Stiffness: A Focus on Vascular Calcification and Its Link to Bone Mineralization. (Arteriosclerosis, thrombosis, and vascular biology 2020) · cited 262x in the literature
"In relation to diabetes mellitus, the regulation of both hyperglycemia and increased protein glycosylation, by AGEs (advanced glycation end products) and O -linked β-N-acetylglucosamine modification, and its role in enhancing intracellular pathophysiological signaling that promotes osteogenic differentiation and calcification of vascular smooth muscle cells are discussed." (abstract, results, passage verified)
pubmedfull study (doi) - supports: From diabetic foot to dementia: A neurovascular continuum linking systemic diabetic vascul… (Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2026)
"Diabetes induces widespread vascular alterations, including endothelial dysfunction, arterial stiffening, oxidative stress, and chronic low-grade inflammation [3,4]... Increased arterial stiffness may impair the Windkessel effect and facilitate the transmission of excessive pulsatile energy into fragile cerebral perforating arteries, thereby promoting microvascular injury and white matter damage" (abstract, results)
pubmedfull study (doi)
Low blood flow is the number one brain imaging predictor of Alzheimer's disease.
"Blood flow—low blood flow is the number one brain imaging predictor of Alzheimer's disease." (said at 0:56:00)
Low cerebral blood flow (hypoperfusion, typically assessed via SPECT or arterial spin labeling MRI) is not the leading or "number one" neuroimaging predictor of Alzheimer's disease. In clinical diagnostic frameworks and comparative imaging studies, pathological hallmark imaging (amyloid-beta PET and tau PET), fluorodeoxyglucose (FDG) PET, and structural MRI (such as medial temporal lobe and hippocampal volumetry) are the primary, most accurate imaging biomarkers for Alzheimer's disease. While characteristic patterns of hypoperfusion (particularly in the posterior cingulate and temporoparietal cortices) are observed in Alzheimer's disease and can assist in differential diagnosis or prognostication of mild cognitive impairment, systematic reviews and comparative studies demonstrate that FDG-PET and specific amyloid/tau imaging biomarkers consistently demonstrate higher diagnostic accuracy and predictive power than perfusion imaging.
- contradicts: A comparison of FDG-PET and blood flow SPECT in the diagnosis of neurodegenerative dementi… (International journal of geriatric psychiatry 2014) · cited 72x in the literature
"Published studies of SPECT accuracy show that it is a useful tool for differential diagnosis, with sensitivities of 65-85% for diagnosing Alzheimer's disease (AD) and specificities (for other neurodegenerative dementias) of 72-87%. PET studies generally report higher accuracy, with sensitivities of 75-99% for AD and specificities of 71-93%." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Systematic review and meta-analysis of diagnostic test accuracy (DTA) studies: the role of… (Annals of palliative medicine 2022) · cited 9x in the literature
"The meta-analysis results showed that the sensitivity and specificity of FDG-PET imaging was significantly higher than those of SPECT and MRI imaging, and the differences were statistically significant (P<0.05)." (abstract, results, passage verified)
pubmedfull study (doi) - contradicts: Prognostic Value of A/T/N Biomarkers: Comparing Plasma and Imaging Modalities in Alzheimer… (Clinical nuclear medicine 2025) · cited 1x in the literature
"Among 1,614 plasma cohort and 130 imaging subcohort participants, tau markers demonstrated the strongest predictive value... suggesting that combinations of amyloid and tau PET captures the most relevant prognostic information." (abstract, results)
pubmedfull study (doi)
Forty percent of 40-year-old men begin to complain of erectile dysfunction.
"And get this: 40% of men at 40 years old start to complain of erectile dysfunction." (said at 0:56:10)
Data from the landmark Massachusetts Male Aging Study (MMAS) established that approximately 40% of men at age 40 experience some degree of erectile dysfunction (with an overall prevalence of 52% across men aged 40 to 70). However, this figure includes mild or minimal erectile difficulties; severe or complete erectile dysfunction affects only about 5% of men at age 40, increasing with age.
A study by Daniel Amen in the Journal of Alzheimer's Disease found that overweight and obese NFL players had lower blood flow in the prefrontal cortex compared to normal-weight players.
"So I actually did a study—I published a study in the Journal of Alzheimer's Disease in my NFL group, and we looked at NFL players who were overweight or obese versus those who were at a healthy weight. The overweight and obese one had low blood flow in their prefrontal cortex" (said at 0:59:30)
Daniel Amen published a study in the Journal of Alzheimer's Disease (2020) examining regional cerebral blood flow via brain SPECT scans across BMI categories (underweight, normal weight, overweight, obese, morbidly obese). The study showed that higher BMI correlated with reduced cerebral blood flow across virtually all brain regions, including the prefrontal cortex and areas implicated in Alzheimer's disease. However, the speaker conflated this study with his earlier NFL cohort work: the published Journal of Alzheimer's Disease study on obesity and cerebral blood flow was conducted in a general adult psychiatric cohort of 17,721 participants (35,442 scans), not specifically in his NFL player group. As an observational cross-sectional imaging study from a private clinic network, the body of evidence provides low certainty.
Former NFL player Ed White lost 150 pounds participating in Dr. Daniel Amen's NFL weight loss group.
"And we did an NFL weight loss group, which was so much fun for me. I had Big Ed White become Little Ed White. He lost 150 pounds, which was really fun." (said at 1:00:00)
No published record matching the claim that former NFL player Ed White lost 150 pounds in Dr. Daniel Amen's weight loss group was located; this does not prove the claim false. Dr. Amen published a study detailing an open-label multi-component intervention in 30 retired NFL players that included weight loss where appropriate (PMID 21615001), but individual player identities and specific weight loss figures such as 150 pounds were not reported in peer-reviewed publications.
In the United States population, 72% are overweight, 42% are obese, and 50% are diabetic or pre-diabetic according to published JAMA data.
"And what is it, 72% of the population is now overweight, 42% obese, 50% are diabetic or pre-diabetic, that was published in JAMA." (said at 1:00:15)
Published nationally representative epidemiological data (primarily from the National Health and Nutrition Examination Survey [NHANES], frequently reported in JAMA and CDC publications) support these figures for US adults. In a landmark JAMA analysis of NHANES data (Menke et al., 2015), the unadjusted prevalence among US adults was 14.3% for total diabetes (diagnosed and undiagnosed) and 38.0% for prediabetes, totaling 52.3% (over 50%) with diabetes or prediabetes. Similarly, NHANES surveillance data show that approximately 71% to 73% of US adults are classified as overweight or obese (BMI ≥25 kg/m²), with adult obesity prevalence (BMI ≥30 kg/m²) reaching approximately 42.4%.
- supports: Prevalence of and Trends in Diabetes Among Adults in the United States, 1988-2012. (JAMA 2015) · cited 2412x in the literature
"In the overall 2011-2012 population, the unadjusted prevalence (using the hemoglobin A1c, FPG, or 2-hour PG definitions for diabetes and prediabetes) was 14.3% (95% CI, 12.2%-16.8%) for total diabetes, 9.1% (95% CI, 7.8%-10.6%) for diagnosed diabetes, 5.2% (95% CI, 4.0%-6.9%) for undiagnosed diabetes, and 38.0% (95% CI, 34.7%-41.3%) for prediabetes" (abstract, results, passage verified)
pubmedfull study (doi)
Adipose tissue converts testosterone into forms of estrogen.
"If you're overweight, your hormone balance isn't right because fat takes healthy testosterone, turns it into unhealthy forms of estrogen." (said at 1:00:39)
Adipose tissue expresses the enzyme aromatase (CYP19A1), which catalyzes the peripheral conversion of androgens, such as testosterone and androstenedione, into estrogens (primarily 17β-estradiol and estrone). In overweight and obese individuals, increased adipose tissue volume and elevated aromatase activity lead to higher conversion rates of testosterone into estrogens, contributing to obesity-related male hypogonadism and altered sex hormone balance.
- supports: Adipose Tissue Dysfunction and Obesity-Related Male Hypogonadism. (International journal of molecular sciences 2022) · cited 124x in the literature
"Several mechanisms may indeed negatively affect the hypothalamic-pituitary-gonadal health, such as higher testosterone conversion to estradiol by aromatase activity in the adipose tissue, increased ROS production, and the release of several endocrine molecules affecting the hypothalamus-pituitary-testis axis" (abstract, passage verified)
pubmedfull study (doi) - supports: Altered Expression of Aromatase and Estrogen Receptors in Adipose Tissue From Men With Obe… (The Journal of clinical endocrinology and metabolism 2025) · cited 34x in the literature
"Aromatase (ARO) converts testosterone into E2, and this occurs mainly in adipose tissue in men... Elevated ARO in SAT was found in obese men, and this was linked to insulin resistance and glycemia, supporting the idea that local estrogen production contributes to metabolic dysregulation." (abstract, results and conclusions)
pubmedfull study (doi) - supports: Metabolic impact of endogenously produced estrogens by adipose tissue in females and males… (Frontiers in endocrinology 2025) · cited 22x in the literature
"Estrogens, comprised primarily of estrone (E1) and estradiol (E2) within WAT, are biosynthesized from circulating androgens androstenedione (A4) and testosterone (T) by aromatase (CYP19A1), which is highly expressed in human and mouse adipose tissue." (abstract, passage verified)
pubmedfull study (doi)
A published study by Daniel Amen examining 35,000 brain scans found a linear correlation where higher body weight was associated with decreased blood flow across virtually every brain region.
"I published a study last year on 35,000 scans showing there was, David, a linear correlation: as your weight went up, blood flow to virtually every area of your brain went down." (said at 1:00:52)
A 2020 cross-sectional study by Daniel Amen and colleagues analyzed 35,442 brain SPECT scans from 17,721 adults in a psychiatric clinic cohort across different BMI categories. The study reported that higher BMI was significantly correlated with decreased cerebral blood flow (hypoperfusion) during both resting and concentration tasks across virtually all 128 brain regions examined. Because this was a retrospective, cross-sectional observational study in a self-selected clinical population, it demonstrates association rather than direct causation.
Fact-checked episodes
Publications
- Examining comorbid and transdiagnostic depression clinical outcomes across anxiety, autism, attention deficit hyperactivity disorder (ADHD), bipolar disorder, depression, and schizotypal personality groups: a novel NeuroMark SPECT approach.medRxiv : the preprint server for health sciences 2026 · CEBM Level 4
- A Replicable NeuroMark Template for Whole-Brain SPECT Reveals Data-Driven Perfusion Networks and Their Alterations in Schizophrenia.Neuroinformatics 2026 · CEBM Level 4
- Classifying schizophrenia patients and healthy individuals: Whole brain SPECT functional connectivity using support vector machine classification.Neuroimage. Reports 2026 · CEBM Level 4
- Functional vs Structural Cortical Deficit Pattern Biomarkers for Major Depressive Disorder.JAMA psychiatry 2025 · CEBM Level 4
- Predicting Regional Cerebral Blood Flow Using Voxel-Wise Resting-State Functional MRI.Brain sciences 2025 · CEBM Level 4
- A multi-site 99m Tc-HMPAO SPECT study of cerebral blood flow in a community sample of patients with major depression.Translational psychiatry 2024 · CEBM Level 4
- Adverse childhood experiences, brain function, and psychiatric diagnoses in a large adult clinical cohort.Frontiers in psychiatry 2024 · CEBM Level 4
- SPECT Functional Neuroimaging Distinguishes Adult Attention Deficit Hyperactivity Disorder From Healthy Controls in Big Data Imaging Cohorts.Frontiers in psychiatry 2021 · CEBM Level 4
- A New Way Forward: How Brain SPECT Imaging Can Improve Outcomes and Transform Mental Health Care Into Brain Health Care.Frontiers in psychiatry 2021 · CEBM Level 5
- Patterns of Regional Cerebral Blood Flow as a Function of Obesity in Adults.Journal of Alzheimer's disease : JAD 2020 · CEBM Level 4
- Deficits in Regional Cerebral Blood Flow on Brain SPECT Predict Treatment Resistant Depression.Journal of Alzheimer's disease : JAD 2018 · CEBM Level 4
- Patterns of Regional Cerebral Blood Flow as a Function of Age Throughout the Lifespan.Journal of Alzheimer's disease : JAD 2018 · CEBM Level 4
- Discriminative Properties of Hippocampal Hypoperfusion in Marijuana Users Compared to Healthy Controls: Implications for Marijuana Administration in Alzheimer's Dementia.Journal of Alzheimer's disease : JAD 2017 · CEBM Level 4
- Classification of Depression, Cognitive Disorders, and Co-Morbid Depression and Cognitive Disorders with Perfusion SPECT Neuroimaging.Journal of Alzheimer's disease : JAD 2017 · CEBM Level 4
- Quantitative Erythrocyte Omega-3 EPA Plus DHA Levels are Related to Higher Regional Cerebral Blood Flow on Brain SPECT.Journal of Alzheimer's disease : JAD 2017 · CEBM Level 4
- Gender-Based Cerebral Perfusion Differences in 46,034 Functional Neuroimaging Scans.Journal of Alzheimer's disease : JAD 2017 · CEBM Level 4
- Perfusion Neuroimaging Abnormalities Alone Distinguish National Football League Players from a Healthy Population.Journal of Alzheimer's disease : JAD 2016 · CEBM Level 4
- Functional neuroimaging with default mode network regions distinguishes PTSD from TBI in a military veteran population.Brain imaging and behavior 2015 · CEBM Level 4
- Functional Neuroimaging Distinguishes Posttraumatic Stress Disorder from Traumatic Brain Injury in Focused and Large Community Datasets.PloS one 2015 · CEBM Level 4
- Clinical comparison of 99mTc exametazime and 123I Ioflupane SPECT in patients with chronic mild traumatic brain injury.PloS one 2014 · CEBM Level 4
- Clinical utility of SPECT neuroimaging in the diagnosis and treatment of traumatic brain injury: a systematic review.PloS one 2014 · CEBM Level 1
- It's time to stop flying blind: how not looking at the brain leads to missed diagnoses, failed treatments, and dangerous behaviors.Alternative therapies in health and medicine 2013 · CEBM Level 4
- Multi-site six month outcome study of complex psychiatric patients evaluated with addition of brain SPECT imaging.Advances in mind-body medicine 2013 · CEBM Level 3
- Effects of brain-directed nutrients on cerebral blood flow and neuropsychological testing: a randomized, double-blind, placebo-controlled, crossover trial.Advances in mind-body medicine 2013 · CEBM Level 2
- Daniel Amen, MD: healing brain injury and damage from environmental toxins. Interviewed by Karen Burnett.Advances in mind-body medicine 2013 · CEBM Level 5
- A phase I study of low-pressure hyperbaric oxygen therapy for blast-induced post-concussion syndrome and post-traumatic stress disorder.Journal of neurotrauma 2012 · CEBM Level 4
- Daniel Amen, MD: the impact of brain imaging on psychiatry and treatment for improving brain health and function. Interview by Karen Burnett.Alternative therapies in health and medicine 2012 · CEBM Level 5
- The clinical utility of brain SPECT imaging in process addictions.Journal of psychoactive drugs 2012 · CEBM Level 5
- Specific ways brain SPECT imaging enhances clinical psychiatric practice.Journal of psychoactive drugs 2012 · CEBM Level 4
- Impact of playing American professional football on long-term brain function.The Journal of neuropsychiatry and clinical neurosciences 2011 · CEBM Level 4
- Elevated BMI is associated with decreased blood flow in the prefrontal cortex using SPECT imaging in healthy adults.Obesity (Silver Spring, Md.) 2011 · CEBM Level 4
- Reversing brain damage in former NFL players: implications for traumatic brain injury and substance abuse rehabilitation.Journal of psychoactive drugs 2011 · CEBM Level 3
- Brain SPECT Imaging in Complex Psychiatric Cases: An Evidence-Based, Underutilized Tool.The open neuroimaging journal 2011 · CEBM Level 5
- Cerebral blood flow differences between long-term meditators and non-meditators.Consciousness and cognition 2010 · CEBM Level 4
- High resolution brain SPECT imaging in a clinical substance abuse practice.Journal of psychoactive drugs 2010 · CEBM Level 5
- Brain SPECT imaging in clinical practice.The American journal of psychiatry 2010 · CEBM Level 5
- Cerebral blood flow changes during chanting meditation.Nuclear medicine communications 2009 · CEBM Level 3
- A comparative analysis of completed suicide using high resolution brain SPECT imaging.The Journal of neuropsychiatry and clinical neurosciences 2009 · CEBM Level 4
- Omentum transposition surgery for patients with Alzheimer's disease: a case series.Neurological research 2008 · CEBM Level 4
- Predicting positive and negative treatment responses to stimulants with brain SPECT imaging.Journal of psychoactive drugs 2008 · CEBM Level 4
- Preliminary evidence differentiating ADHD using brain SPECT imaging in older patients.Journal of psychoactive drugs 2008 · CEBM Level 4
- An analysis of regional cerebral blood flow in impulsive murderers using single photon emission computed tomography.The Journal of neuropsychiatry and clinical neurosciences 2007 · CEBM Level 4
- High-resolution brain SPECT imaging and eye movement desensitization and reprocessing in police officers with PTSD.The Journal of neuropsychiatry and clinical neurosciences 2005 · CEBM Level 4