John Hussman | |
---|---|
Born | John Peter Hussman October 15, 1962 |
Nationality | American |
Alma mater | Northwestern University (BSc, MS) Stanford University (PhD) |
Occupations | Prof. International Finance University of Michigan (1992–98)
|
Known for | Founder, Hussman Strategic Advisors |
Spouse | Theresa "Terri" Hussman [1] |
Children | 4 |
Website | https://www.hussman.com |
John Peter Hussman (born 15 October 1962), is an American philanthropist, economist, and hedge fund manager.
Hussman holds a PhD in economics from Stanford University, as well as a master's degree in education and social policy and a bachelor's degree in economics from Northwestern University.
From 1992 to 1998, he was Professor of Economics and International Finance at the University of Michigan.[ citation needed ]
In the mid-1980s, Hussman worked as an options mathematician for Peters & Company at the Chicago Board of Trade, and in 1988 founded his investment company, now known as Hussman Strategic Advisors. [2] After spending much of the early-1990s as a "lonely raging bull", [3] he became increasingly bearish in the late-1990's. [4] He successfully anticipated the collapse of dot-com bubble, as well as the 2008–09 global financial crisis, then reversed his view about valuations after the market collapse in late-2008, declaring “U.S. stocks are now undervalued”. [5]
By September 2010, Hussman managed US$6.7 billion. However, between 2013 and 2017, he became increasingly bearish, asserting that the "quantitative easing" ("QE") and zero interest rate policies of the Federal Reserve had contributed to a “hypervalued market”, [6] Hussman's investment performance suffered as a result, and he was labeled a “permabear”. His performance during this period sharply lagged the S&P 500, in contrast to the years prior to 2013. By late-2017, assets under management had declined to US$1 billion. Hussman has regularly commented on his error during that period, [7] tracing it to his insistence on stress-testing his methods against Depression-era data following the global financial crisis, which led him to emphasize the importance of “overvalued, overbought, overbullish” conditions that had historically been reliable indications of market tops. [8] In late-2017, he gave up, saying "Evidently, once interest rates hit zero, so did the collective IQ of Wall Street". [9]
Hussman is known for a strongly quantitative approach to macro-investing and publishes a regular market comment freely available on his website, that updates his projections of 10-12 year returns for the S&P 500, which remained below 0% from 2015 until early-2020, when the market plunged in response to the COVID-19 pandemic. [10] In July 2017, Hussman said that markets were "at the most offensive level of overvaluation in history" — beyond even 1929 and 2000". In June 2018, he projected a market decline in excess of 64% (two-thirds) by the trough of the market cycle. He reiterated that projection of a two-thirds market loss in November 2020, after a rebound in the S&P 500 back to its pre-pandemic highs. [11]
As he did in 2000, at the peak of the technology bubble [ Hussman Investment Research & Insight, October 3, 2000 ] and in 2007, before the global financial crisis [ Market Internals Go Negative, July 30, 2007 ], Hussman regularly emphasizes that his statements about valuations are not near-term forecasts, and that bubbles can only occur when investors ignore overvaluation for years. In practice, he says, “In addition to valuations, which inform us about long-term returns and full-cycle risks, we consider the uniformity or divergence of market internals, to infer whether investors are inclined toward speculation or toward risk-aversion.” Hussman argues that the worst market losses occur when both are unfavorable, opening a “trap door.” [12] .
In 1998, Hussman left academic economics to increase his focus on philanthropic efforts, using his ongoing investing work to fund charitable projects in autism, global health, education, displaced populations, homelessness, and research focused on the genetics and biology of complex conditions such as autism and multiple sclerosis. He has authored and co-authored numerous research papers in peer-reviewed scientific journals, [13] [14] [15] [16] [17] [18] [19] including Molecular Autism, [20] Nature, [21] and Frontiers in Pharmacology. [22]
In 2001, Hussman proposed what is now known as the “excitatory/inhibitory” theory of autism in the Journal of Autism and Developmental Disorders. Drawing on evidence from genetic, neuroanatomical, and neurobiological research, he proposed: "Although it is possible that the breadth of impairments in autism are caused by multiple defects in relatively independent systems, autism may instead reflect dysfunction in a single factor shared in common by many systems. Specifically, the severe disruptions observed in autism may be linked to suppression of GABAergic inhibition, resulting in excessive stimulation of glutamate-specialized neurons and loss of sensory gating. This view recognizes the possibility of multiple etiologies in autism. That is, there may exist a spectrum of genetic and environmental factors which impair inhibitory tone. Loss of inhibitory control from GABAergic neurons may result in hyperexcitation of vulnerable target neurons. Such a model may provide a reasonable characterization of autism." [23] [24] [25] Rubenstein and Merzenich later cited Hussman's work in 2003, increasing attention to the hypothesis, and stating it in terms of an increased ratio of excitation to inhibition (E/I). [26] This mechanism has since become a well-established line of research in the autism field.
In 2012, Hussman founded the Hussman Institute for Autism. The Institute's programs focus on advancing translational research on the genetics and neurobiology of autism, and on developing a continuum of resources to provide positive support to individuals with autism, including training materials, model programs, and research-based practices. [27] In 2021, the Institute relocated its research laboratories to Florida, adjacent to the Hussman Institute for Human Genomics at the University of Miami. [28]
Hussman has served on non-profit boards of institutions including the University of Miami, the Baudhuin School for Autism at Nova Southeastern University, and the Autism Society of America. Hussman and his wife Terri also serve on the boards of Maryland charities including the Light House Homelessness Prevention Center, and Hospice of the Chesapeake. Hussman was chosen as the 2013 Philanthropist of the Year by the AFP. [29] [30]
The striatum, or corpus striatum, is a nucleus in the subcortical basal ganglia of the forebrain. The striatum is a critical component of the motor and reward systems; receives glutamatergic and dopaminergic inputs from different sources; and serves as the primary input to the rest of the basal ganglia.
γ-Aminobutyric acid, or GABA, is the chief inhibitory neurotransmitter in the developmentally mature mammalian central nervous system. Its principal role is reducing neuronal excitability throughout the nervous system.
SLITRK1 is a human gene that codes for a transmembrane and signalling protein that is part of the SLITRK gene family, which is responsible for synapse regulation and presynaptic differentiation in the brain. Expression of the gene has been linked to early formation of excitatory synapses through binding with receptor tyrosine phosphatase PTP (LAR-RPTP). Various studies over the years have linked mutations in the gene to conditions on the OCD spectrum, Tourette syndrome and trichotillomania, however the mutations in the genome itself vary greatly between individuals, with most mutations observed being hard to find in repeat studies.
The heritability of autism is the proportion of differences in expression of autism that can be explained by genetic variation; if the heritability of a condition is high, then the condition is considered to be primarily genetic. Autism has a strong genetic basis. Although the genetics of autism are complex, autism spectrum disorder (ASD) is explained more by multigene effects than by rare mutations with large effects.
Gamma-aminobutyric acid receptor subunit beta-3 is a protein that in humans is encoded by the GABRB3 gene. It is located within the 15q12 region in the human genome and spans 250kb. This gene includes 10 exons within its coding region. Due to alternative splicing, the gene codes for many protein isoforms, all being subunits in the GABAA receptor, a ligand-gated ion channel. The beta-3 subunit is expressed at different levels within the cerebral cortex, hippocampus, cerebellum, thalamus, olivary body and piriform cortex of the brain at different points of development and maturity. GABRB3 deficiencies are implicated in many human neurodevelopmental disorders and syndromes such as Angelman syndrome, Prader-Willi syndrome, nonsyndromic orofacial clefts, epilepsy and autism. The effects of methaqualone and etomidate are mediated through GABBR3 positive allosteric modulation.
The GABAA beta-2 subunit is a protein that in humans is encoded by the GABRB2 gene. It combines with other subunits to form the ionotropic GABAA receptors. GABA system is the major inhibitory system in the brain, and its dominant GABAA receptor subtype is composed of α1, β2, and γ2 subunits with the stoichiometry of 2:2:1, which accounts for 43% of all GABAA receptors. Alternative splicing of the GABRB2 gene leads at least to four isoforms, viz. β2-long (β2L) and β2-short. Alternatively spliced variants displayed similar but non-identical electrophysiological properties. GABRB2 is subjected to positive selection and known to be both an alternative splicing and a recombination hotspot; it is regulated via epigenetic regulation including imprinting and gene and promoter methylation GABRB2 has been associated with a number of neuropsychiatric disorders, and found to display altered expression in cancer.
Homeobox protein engrailed-2 is a protein that in humans is encoded by the EN2 gene. It is a member of the engrailed gene family.
Myotilin is a protein that in humans is encoded by the MYOT gene. Myotilin also known as TTID is a muscle protein that is found within the Z-disc of sarcomeres.
VPS13A is a protein that in humans is encoded by the VPS13A gene.
Calcium-binding mitochondrial carrier protein Aralar1 is a protein that in humans is encoded by the SLC25A12 gene. Aralar is an integral membrane protein located in the inner mitochondrial membrane. Its primary function as an antiporter is the transport of cytoplasmic glutamate with mitochondrial aspartate across the inner mitochondrial membrane, dependent on the binding of one calcium ion. Mutations in this gene cause early infantile epileptic encephalopathy 39 (EIEE39), symptomized by global hypomyelination of the central nervous system, refractory seizures, and neurodevelopmental impairment. This gene has connections to autism.
Neuroligin (NLGN), a type I membrane protein, is a cell adhesion protein on the postsynaptic membrane that mediates the formation and maintenance of synapses between neurons. Neuroligins act as ligands for β-neurexins, which are cell adhesion proteins located presynaptically. Neuroligin and β-neurexin "shake hands", resulting in the connection between two neurons and the production of a synapse. Neuroligins also affect the properties of neural networks by specifying synaptic functions, and they mediate signalling by recruiting and stabilizing key synaptic components. Neuroligins interact with other postsynaptic proteins to localize neurotransmitter receptors and channels in the postsynaptic density as the cell matures. Additionally, neuroligins are expressed in human peripheral tissues and have been found to play a role in angiogenesis. In humans, alterations in genes encoding neuroligins are implicated in autism and other cognitive disorders. Antibodies in a mother from previous male pregnancies against neuroligin 4 from the Y chromosome increase the probability of homosexuality in male offspring.
Phospholipase D family, member 5 is a protein that in humans is encoded by the PLD5 gene.
Brett Abrahams is an American geneticist and neuroscientist involved in the identification and subsequent functional characterization of the autism-related gene CNTNAP2 at UCLA. Abrahams is an assistant professor at the Albert Einstein College of Medicine in New York City.
Autism spectrum disorder (ASD) refers to a variety of conditions typically identified by challenges with social skills, communication, speech, and repetitive sensory-motor behaviors. The 11th International Classification of Diseases (ICD-11), released in January 2021, characterizes ASD by the associated deficits in the ability to initiate and sustain two-way social communication and restricted or repetitive behavior unusual for the individual's age or situation. Although linked with early childhood, the symptoms can appear later as well. Symptoms can be detected before the age of two and experienced practitioners can give a reliable diagnosis by that age. However, official diagnosis may not occur until much older, even well into adulthood. There is a large degree of variation in how much support a person with ASD needs in day-to-day life. This can be classified by a further diagnosis of ASD level 1, level 2, or level 3. Of these, ASD level 3 describes people requiring very substantial support and who experience more severe symptoms. ASD-related deficits in nonverbal and verbal social skills can result in impediments in personal, family, social, educational, and occupational situations. This disorder tends to have a strong correlation with genetics along with other factors. More research is identifying ways in which epigenetics is linked to autism. Epigenetics generally refers to the ways in which chromatin structure is altered to affect gene expression. Mechanisms such as cytosine regulation and post-translational modifications of histones. Of the 215 genes contributing, to some extent in ASD, 42 have been found to be involved in epigenetic modification of gene expression. Some examples of ASD signs are specific or repeated behaviors, enhanced sensitivity to materials, being upset by changes in routine, appearing to show reduced interest in others, avoiding eye contact and limitations in social situations, as well as verbal communication. When social interaction becomes more important, some whose condition might have been overlooked suffer social and other exclusion and are more likely to have coexisting mental and physical conditions. Long-term problems include difficulties in daily living such as managing schedules, hypersensitivities, initiating and sustaining relationships, and maintaining jobs.
Martha Herbert is an American physician and assistant professor of neurology at Harvard Medical School and pediatric neurologist at Massachusetts General Hospital. Herbert is also director of the TRANSCEND program at the Athinoula A. Martinos Center for Biomedical Imaging.
Hypofrontality is a state of decreased cerebral blood flow (CBF) in the prefrontal cortex of the brain. Hypofrontality is symptomatic of several neurological medical conditions, such as schizophrenia, attention deficit hyperactivity disorder (ADHD), bipolar disorder, and major depressive disorder. This condition was initially described by Ingvar and Franzén in 1974, through the use of xenon blood flow technique with 32 detectors to image the brains of patients with schizophrenia. This finding was confirmed in subsequent studies using the improved spatial resolution of positron emission tomography with the fluorodeoxyglucose (18F-FDG) tracer. Subsequent neuroimaging work has shown that the decreases in prefrontal CBF are localized to the medial, lateral, and orbital portions of the prefrontal cortex. Hypofrontality is thought to contribute to the negative symptoms of schizophrenia.
Metadoxine, also known as pyridoxine-pyrrolidone carboxylate, is a drug used to treat chronic and acute alcohol intoxication. Metadoxine accelerates alcohol clearance from the blood.
Joseph D. Buxbaum is an American molecular and cellular neuroscientist, autism researcher, and the Director of the Seaver Autism Center at the Icahn School of Medicine at Mount Sinai. Buxbaum is also, along with Simon Baron-Cohen, the co-editor of the BioMed Central journal Molecular Autism, and is a member of the scientific advisory board of the Autism Science Foundation. Buxbaum is a Professor of Psychiatry, Neuroscience, and Genetics and Genomic Sciences. He is also the Vice Chair for Research and for Mentoring in the Department of Psychiatry at the Icahn School of Medicine at Mount Sinai.
Margaret Ann Pericak-Vance is an American human geneticist who is the Dr. John T. Macdonald Foundation Professor of Human Genetics and director of the John P. Hussman Institute for Human Genomics at the University of Miami. She is known for her research on the genetics of common human diseases. This research has led to a number of findings of genes that increase the risk of certain diseases, such as apolipoprotein E and Alzheimer's disease, IL7R and multiple sclerosis, and complement factor H and macular degeneration.
Presynaptic inhibition is a phenomenon in which an inhibitory neuron provides synaptic input to the axon of another neuron to make it less likely to fire an action potential. Presynaptic inhibition occurs when an inhibitory neurotransmitter, like GABA, acts on GABA receptors on the axon terminal. Or when endocannabinoids act as retrograde messengers by binding to presynaptic CB1 receptors, thereby indirectly modulating GABA and the excitability of dopamine neurons by reducing it and other presynaptic released neurotransmitters. Presynaptic inhibition is ubiquitous among sensory neurons.