Office: PCD 4105
- Curriculum Vitae
- Recent Publications
- Research on Health and Nutrition
- Myths and Mischief in Medical Research Powerpoint
- Myths and Mischief in Medical Research Syllabus
- Research on Why Parents Forget Children in Hot Cars
- Dr. Diamond’s podcast on heart disease with responses by cardiologists
- Diet and Heart Disease Research
Ph.D. Area: Cognitive & Neural Sciences
Highlights: Physiology of Behavior, Psychology of Learning, Neurobiology of Memory, Disturbance of Brain and Behavior by Stress.
Research on Auditory System Plasticity and Memory (1980-1989)
My dissertation research characterized plasticity of single cell activity in the auditory cortex during learning. The issue we addressed was the functional significance of neural plasticity in a sensory system. How is it possible for a cell to represent the physical parameters of sound, as well as its psychological significance? One component of this work was to review the functional neuroanatomy of the thalamo-cortical auditory system. We described the parallel pathways that carried purely sensory information in parallel with psychological information to the auditory cortex. In empirical work we directly measured single cell activity in the auditory cortex during classical conditioning in awake cats. Our research demonstrated, for the first time, that the sensory cortical maps were capable of demonstrating plasticity in their representation. We demonstrated that individual auditory cortical neurons could exhibit rapid and systematic changes in their receptive fields in response to perceived changes in the significance of sounds.
Subset of Publications
Diamond, D.M. and Weinberger, N.M. (1984) Physiological plasticity of single neurons in auditory cortex of the cat during acquisition of the pupillary dilation conditioned response: II. Secondary field (AII). Behavioral Neuroscience, 98:189‑210.
Diamond, D.M. and Weinberger, N.M. (1986) Classical conditioning rapidly induces specific changes in frequency receptive fields of single neurons in secondary and ventral ectosylvian auditory cortical fields. Brain Research, 372:357‑360.
Weinberger, N.M. and Diamond, D.M. (1987) Physiological plasticity of single neurons in auditory cortex: Rapid induction by learning. Progress in Neurobiology, 27:1‑55.
Animal Model of Alzheimer’s Disease (2000-2010)
I collaborated with a group at USF that studied doubly transgenic mAPP+mPS1 mice, which serve as an animal model of Alzheimer’s disease (AD). These mice develop an age-related impairment of cognitive function in a spatial learning and memory task that I devised, which combined features of a water maze and a radial arm maze. We showed that nontransgenic mice learned a new hidden platform location each day and then exhibited intact memory for the platform location in a retention trial. In contrast, older transgenic mice were unable to improve their performance in finding the hidden platform over trials. We found that the cognitive performance of individual mice within the transgenic group were inversely related to the amount of amyloid deposited in the frontal cortex and hippocampus. In addition, we performed a series of studies assessing the effects of a vaccine for amyloid, which cleared cortical amyloid and improved cognition. This research has served as a useful behavioral approach toward evaluating the functional consequences of potential AD therapies, especially those designed to reduce amyloid load.
Subset of Publications
Morgan, D., Diamond, D.M., Gottschall, P., Ugen, K., Dickey, C., Hardy, J., Jantzen, P., DiCarlo, G., Wilcock, D., Connor, K., King, D., Hatcher, J., Canals, K., Gordon, M. and Arendash, G. (2000) Vaccination with Aß peptide prevents the development of age-related memory deficits in an animal model of Alzheimer’s disease. Nature, 408:982-985.
King, D.L., Arendash, G.W., Gordon, M.N., Morgan, D., Jantzen, P., Hope, C., Hatcher, J. and Diamond, D.M. (2001) Progressive, age-related behavioral impairments in transgenic mice carrying both mutant amyloid precursor protein (APP) and presenilin 1 (PS1) transgenes. Brain Research, 891:42-53.
Gordon, M.N., King, D.L., Diamond, D.M., Morgan, D., Jantzen, P., Hope, C., Hatcher, J. and Arendash, G.W. (2001) Correlation between working memory deficits and cortical aß deposition in transgenic APP+PS1 mice. Neurobiology of Aging, 22:377-385.
Arendash, G.W., Gordon, M.N., Diamond, D.M., Austin, L.A., Hatcher, J., Jantzen, P., DiCarlo, G., Wilcock, D. and Morgan, D. (2001) Behavioral assessment of Alzheimer’s transgenic mice following long-term Ab vaccination: Task specificity and correlations with extent of Ab deposition. DNA and Cell Biology, 20:737-744.
Dickey, C.A., Gordon, M.N., Mason, J., Wilson, N.J, Diamond, D.M., Guzowski, J.F. and Alamed, J., Wilcock, D.M, Diamond, D.M., Gordon, M.N., Morgan, D. (2006) Two-day radial-arm water maze learning and memory task; robust resolution of amyloid related memory deficits in transgenic mice. Nature Protocols, 1:1671-1769.
Morgan, D., Munireddy, S., Alamed, J., DeLeon, Diamond, D.M., Bickford, P., Hutton, M., Lewis, J., McGowan, E. and Gordon, M.N. (2008) Apparent behavioral benefits of tau overexpression in P301L tau transgenic mice. Journal of Alzheimer’s Disease, 15:605-614.
Research on Stress and Brain Plasticity (1986-2016)
I have studied the effects of stress on hippocampal synaptic plasticity, in vitro and in vivo. We discovered that exposing rats to a stressful environment blocked the expression of synaptic plasticity in the hippocampus. We extended the preliminary findings to include the use of a live cat as an ethologically relevant stressor to rats. Exposure of rats to a cat produced a profound stress response which blocked synaptic plasticity in the hippocampus in behaving rats, as well as in the hippocampus, in vitro. We also found that cat exposure enhanced plasticity in the amygdala. This work provides insight into how memory-related synaptic plasticity in the brain is modulated by stress.
Subset of Publications
Diamond, D.M., Bennett, M.C., Stevens, K.E., Wilson, R.L. and Rose, G.M. (1990) Exposure to a novel environment interferes with the induction of hippocampal primed burst potentiation in behaving rats, Psychobiology, 18:273-281.
Diamond, D.M., Bennett, M.C., Fleshner, M. and Rose, G.M. (1992) Inverted-U relationship between the level of peripheral corticosterone and the magnitude of hippocampal primed burst potentiation, Hippocampus, 2:421-430.
Diamond, D.M., Fleshner, M. and Rose, G.M. (1994) Psychological stress repeatedly blocks hippocampal primed burst potentiation in the behaving rat, Behavioural Brain Research, 62:1-9.
Mesches, M.M., Fleshner, M., Heman, K.L. Rose, G.M. and Diamond, D.M. (1999) Exposing rats to a predator blocks primed burst potentiation in the hippocampus in vitro, Journal of Neuroscience, 19:(RC18) 1-5.
Vouimba, R.M., Muñoz, C., Diamond, D.M. (2006) Differential effects of predator stress and the antidepressant tianeptine on physiological plasticity in the hippocampus and basolateral amygdala. Stress: The International Journal on the Biology of Stress, 9:29-40.
Research on Stress and Memory (1996-2016)
My group has studied the effects of stress on different forms of memory. We have shown that acute stress impaired hippocampus-dependent, but not hippocampus-independent memory. In conjunction with the behavioral work, we have studied molecular mechanisms which are activated by memory, as well as blocked by tee stress-induced impairment of memory. This work provides insight into the complex effects of stress on different forms of memory.
Subset of Publications
Diamond, D.M., Ingersoll, N., Fleshner, M. and Rose, G.M. (1996) Psychological stress impairs spatial working memory: Relevance to electrophysiological studies of hippocampal function, Behavioral Neuroscience, 110: 661-672.
Diamond, D.M., Park, C.R., Heman, K.L. and Rose, G.M. (1999) Exposing rats to a predator impairs spatial working memory in the radial arm water maze, Hippocampus, 9:542-552.
Sandi, C., Woodson, J.C., Haynes, V.F., Park, C.R., Touyarot, K., Lopez-Fernandez, M.A., Venero, C. and Diamond, D.M. (2005) Stress-induced spatial memory impairment is associated with a selective decrease in the expression of NCAM in hippocampus and prefrontal cortex. Biological Psychiatry, 57:856-864.
Zoladz, P.R., Park, C.R., Halonen, J.D., Salim, S., Alzoubi, K.H., Srivareerat, M., Fleshner, M., Alkadhi, K. and Diamond, D.M. (2012) Differential expression of molecular markers of synaptic plasticity in the hippocampus, prefrontal cortex and amygdala in response to spatial learning, predator exposure and stress-induced amnesia. Hippocampus, 22:577-589.
Halonen, J.D., Zoladz, P.R., Park, C.R.. and Diamond, D.M. (2016) Behavioral and neurobiological assessments of predator-based fear conditioning and extinction. Journal of Behavioral and Brain Science, 6:337-356.
Research on Traumatic Memory Processing (2000-Present)
In parallel with our work on stress, memory and brain plasticity, we have assessed the functional significance of stress effects on the hippocampus and amygdala. In theoretical work we have provided a framework for understanding the conceptual basis for how and why stress affects the hippocampus. We published reviews and syntheses on how stress affects the dynamics of information processing. This theoretical framework emphasizes that stress first activates the hippocampus, and then suppresses its plasticity, to produce restricted fragments of memory which are time-locked to the onset of a stressor. In addition, we have discussed the role of hippocampal and amygdala processing in the development of PTS from an evolutionary perspective. Overall, this work enables us to have a better understanding of the neurobiological basis of traumatic memory processing in people diagnosed with PTSD.
Subset of Publications
Diamond, D.M. and Park, (2000) Predator exposure produces retrograde amnesia and blocks synaptic plasticity: Progress toward understanding how the hippocampus is affected by stress. Annals of the New York Academy of Sciences, pp. 453-455.
Diamond, D.M., Park, C.R. and Woodson, J.C. (2004) Stress generates emotional memories and retrograde amnesia by inducing an endogenous form of hippocampal LTP. Hippocampus, 14:281-291.
Diamond, D.M., Park, C.R., Campbell, A.M. and Woodson, J.C. (2005) Competitive interactions between endogenous LTP and LTD in the hippocampus underlie the storage of emotional memories and stress-induced amnesia. Hippocampus 15:1006-1025.
Diamond, D.M. Campbell, A.M., Park, C.R., Halonen, J. and Zoladz, P.R. (2007) The temporal dynamics model of emotional memory processing: A synthesis on the neurobiological basis of stress-induced amnesia, flashbulb and traumatic memories, and the Yerkes-Dodson Law. Neural Plasticity, vol. 2007, Article ID 60803, doi:10.1155/2007/60803.
Diamond, D.M. and Zoladz, P.R., (2016) Dysfunctional or hyperfunctional? The amygdala in PTSD is the bull in the evolutionary china shop. Journal of Neuroscience Research, 94(6): 437-444.
Animal Model of PTSD (2007-2018)
My group incorporated the use of cat exposure in conjunction with daily social instability in rats to study physiological and behavioral features of an animal model of PTSD. This work has taken into account clinical aspects of the behavioral and physiological symptoms commonly observed in traumatized people in our animal model of PTSD. We have found that predator exposure administered in conjunction with social instability produces responses in rats that are comparable to symptoms commonly observed in traumatized people. In addition, we have studied the influence of pharmacological agents on the expression of PTSD-like effects at behavioral and physiological levels of analysis in predator-exposed rats.
Subset of Publications
Zoladz, P.R., Conrad, C.D., Fleshner, M. and Diamond, D.M. (2008) Acute episodes of inescapable predator exposure in conjunction with daily social stress as an animal model of post-traumatic stress disorder. Stress: The International Journal on the Biology of Stress, 11:259-281.
Zoladz, P.R., Fleshner, M. and Diamond, D.M. (2012) Psychosocial animal model of PTSD produces a long-lasting traumatic memory, an increase in general anxiety and PTSD-like glucocorticoid abnormalities. Psychoneuroendocrinology, 37:1541-1545.
Zoladz, P.R., Fleshner, M. and Diamond, D.M. (2013) Differential effectiveness of tianeptine, clonidine and amitriptyline in blocking traumatic memory expression, anxiety and hypertension in an animal model of PTSD. Progress in Neuropsychopharmacology & Biological Psychiatry, 44:1-16.
Zoladz, P.R. and Diamond, D.M. (2015) Psychosocial stress in rats: an animal model of PTSD based on clinically relevant risk factors. In: The Comprehensive Guide to Post-traumatic Stress Disorder, Springer Publishing.
Zoladz, P.R. and Diamond, D.M. (2016) Predator-Based Psychosocial Stress Animal Model of PTSD: Preclinical Assessment of Traumatic Stress at Cognitive, Hormonal, Pharmacological, Cardiovascular and Epigenetic Levels of Analysis. Experimental Neurology, 284:211-219.
Clinical Research on a Cognitive Treatment for PTSD (2012-2018)
In addition to my preclinical research on an animal model of PTSD I have been working with a clinical research group at USF on a novel approach to PTSD treatment. This non-pharmacological approach is referred to as accelerated response therapy (ART), which is a form of eye movement desensitization and reprocessing (EMDR). ART has been shown to be effective in the treatment of individuals with civilian and military forms of PTSD. It focuses on reducing physiologic and emotional reactivity linked to intrusive emotional images and memories of trauma with visualization, relaxation techniques and rescripting of trauma imagery in conjunction with lateral eye movements. The effectiveness of ART as a treatment for PTSD is documented in our numerous publications and in the support of ART by the Department of Defense in the treatment of veterans with PTSD.
Subset of Publications
Kip, K.E., Elk, C.A., Sullivan, K.L., Kadel, R., Lengacher, C.A., Long, C.J., Shuman, A., Rosenzweig, L., Hernandez, D.F., Street, J.D., Girling, S.A., Diamond, D.M. (2012) Brief treatment of symptoms of post-traumatic stress disorder (PTSD) by use of Accelerated Resolution Therapy (ART). Behavioral Sciences; 2(2): 115-134;doi:10.3390/bs2020115.
Kip, K.E., Rosenzweig, L., Hernandez, D.F., Shuman, A., Sullivan, K.L., Long, C., Taylor, J., McGhee, S., Girling,S.A., Wittenberg, T., Sahebzamani, F., Lengacher, C.A., Kadel,R., and Diamond, D.M. (2013) Randomized Controlled Trial of Accelerated Resolution Therapy (ART) for Symptoms of Combat-Related Post-Traumatic Stress Disorder (PTSD). Military Medicine, 178:1298-1309.
Kip, K.E., , Shuman, A., Hernandez, D.F., Diamond, D.M. and Rosenzweig, L (2014) Case report and theoretical description of accelerated resolution therapy (ART) for military-related post-traumatic stress disorder. Military Medicine, 179:31-37.
Kip, K.E., Rosenzweig, L., Hernandez, D.F., Shuman, A., Diamond, D.M., Girling, S.A., Sullivan, K.L., Wittenberg, T., Witt, A.M., Lengacher, C.A., Andeerson, B. and McMillan, S.C. (2015) Comparison of Accelerated Resolution Therapy (ART) for Treatment of Symptoms of PTSD and Sexual Trauma Between Civilian and Military Adults. Military Medicine, 180:964-971.
Kip, K.E., and Diamond, D.M., (2018) Clinical, empirical, and theoretical rationale for selection of accelerated resolution therapy (ART) for treatment of post-traumatic stress disorder in VA and DoD facilities. Military Medicine 183(9-10):E314-E321.
Critiques of Diagnostic Measures of PTSD (2016 – Present)
There are numerous clinical measures that quantify the magnitude and extent of cognitive dysfunction, particularly in the case of psychological trauma. In a series of studies I collaborated with Dr. Zack Cernovski to assess the validity and utility of these measures. In a subset of our papers we critiqued the Modified Somatic Perception Questionnaire (MSPQ), which is often used to diagnose whether an individual is exhibiting trauma symptoms that are legitimately expressed by psychiatric patients, or those injured in motor vehicle accidents, or by injured war veterans, but have been incorrectly labeled as malingering. These patients are particularly vulnerable to being falsely diagnosed as malingerers, which may lead to denials of therapies and of other benefits to the injured patients.
Subset of Publications
Cernovsky, Z., Diamond, D.M., Mendonça, J.D. and Ferrari, J.R. (2020) Inappropriate Use of the Modified Somatic Perception Questionnaire (MSPQ) to Diagnose Malingering. Archives of Psychiatry and Behavioral Sciences. 3:7-12.
Cernovsky, Z., Mann, S., Diamond, D.M., et al. (2020) Critical review of the content validity of the Miller Forensic Assessment of Symptoms Test (M-FAST). Archives of Psychiatry and Behavioral Sciences. 2020;3(2):16-29.
Cernovsky, Z. and Diamond, D.M. (2020) High risk of false classification of injured people as malingerers by the structured inventory of malingered symptomatology (SIMS): A review. Archives of Psychiatry and Behavioral Sciences. 3(2):30-38.
Cernovsky, Z., Mann, S., Diamond, D.M., et al. (2020) Irremediably flawed nature of analog validation methodology of malingering tests. Archives of Psychiatry and Behavioral Sciences. 2020;3(2):39-45.
Cernovsky, Z., Fattahi, M., Litman, L.C. and Diamond, D.M. (2021) Validation of the PTSD Checklist for DSM-5 (PCL-5) on patients injured in car accidents. European Journal of Medical and Health Sciences.
Research on Diet, Cholesterol and Cardiovascular Disease (2002-Present)
For the past 20 years I have studied research which has purportedly demonstrated that consumption of food rich in saturated fat and cholesterol, as well as having elevated serum cholesterol, increases one’s risk of developing heart disease. I have published papers and participated in documentaries which are critical of the dogmatic view that a diet rich in saturated fat and elevated serum cholesterol are atherogenic.
Subset of Publications
Diamond, D.M. and Ravnskov, U. (2015) How statistical deception created the appearance that statins are safe and effective at improving cardiovascular disease outcomes. Expert Review of Clinical Pharmacology. 8(2), 201–210 (doi:10.1586/17512433.2015.1012494).
Ravnskov, U., Diamond, D.M., Hama, R., Hamazaki, T., Hammarskjöld, B., Hynes, N., Kendrick, M., Langsjoen, P.H., Malhotra, A., Mascitelli, L., McCully, K.S., Ogushi, Y., Okuyama, H., Rosch, P.J., Schersten, T., Sultan, S., Sundberg, R. (2016) Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly. A systematic review. BMJ Open. 6;6, e010401; doi: 10.1136/bmjopen-2015-010401
Ravnskov, U., de Lorgeril, M., Diamond, D. M., Hama, R., et al. (2018) LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature. Expert Review of Clinical Pharmacology, 11:959-970.
Diamond, D.M. de Lorgeril, M., Kendrick M., Ravnskov, U., and Rosch, P.J. (2019) Formal comment on “Systematic review of the predictors of statin adherence for the primary prevention of cardiovascular disease”. PLoS ONE 14(1): e0205138. https://doi.org/10.1371/journal.pone.0205138
Diamond, D.M., Alabdulgader, A.A., de Lorgeril, M., Harcombe, Z., Kendrick M., Malhotra, A., O’Neill, B.O., Ravnskov, U., Sultan, S. and Volek, J.S. (2020) Dietary Recommendations for Familial Hypercholesterolaemia: an Evidence-Free Zone. BMJ Evidence-Based Medicine, DOI: 10.1136/bmjebm-2020-111412
Diamond, D.M., O’Neill, B.O. and Volek, J.S. (2020) Low carbohydrate diet: Are concerns with saturated fat, lipids and cardiovascular disease risk justified? Current Opinion in Endocrinology and Diabetes 27: 291-300.
Cognitive and Neurobiological Perspectives on Why Parents and Caretakers Lose Awareness of Children in Cars (2005 - Present)
For almost 2 decades I have studied how normal (i.e., attentive and loving) parents and caretakers, without evidence of abuse or neglect of children, and without evidence of drug abuse or organic brain dysfunction, unintentionally and unknowingly, leave children in cars. Under conditions in which the ambient temperature is warm enough and the car is exposed to direct sunlight, heat builds within the car and the child may die or become brain damaged as a result of hyperthermia. It is difficult to understand how a person can leave a child in a car, and yet, it appears to occur at an alarmingly high rate. I have studied this phenomenon from a neuropsychologucal perspective.
My hypothesis as to how children have been unknowingly and unintentionaly left in cars I was first published in an on-line article in The Conversation, entitled: “An epidemic of children dying in hot cars: a tragedy that can be prevented”. I then described the phenomenon at length in a peer-reviewed publication in which I explained that children forgotten in cars results from: a) the driver loses awareness of the presence of the child in the car; 2) the driver exhibits a failure of the brain’s “prospective memory” system; 3) intervening events during the drive, including stressors and strong distractions, may contribute to the cause of the failure of “prospective memory”; competition between “habit” and “prospective memory” systems.
I have served on federal committees to assess why children are forgotten in cars and how the auto industry can respond to this flaw in human factors. In addition, I have served as an expert witness in cases in which parents have been charged with crimes, such as child abandonment, manslaughter and murder. My expert testimony has enabled judges and juries to understand how attentive and loving parents are capable of forgetting their child in car, which can result in a catastrophe.
Diamond, D.M. (2019) When a child dies of heatstroke after a parent or caretaker, unknowingly, leaves the child in a car: How does it happen and is it a crime?” Medicine, Science and the Law, 59(2):115-26.
CNS (Cognitive Neuroscience)