The happiness gene – is there one?

In recent decades many have observed that certain people are always optimistic.  Naturally, researchers who requested funding to study if “optimism” could be inherited did get some money. Any major answer? The 5-HTT gene family: The feeling of satisfaction is apparently controlled by the 5-HTT gene family. It probably may not be the only gene family that controls the feeling of satisfaction but it has been the one most studied. There are many members in the 5-HTT gene family with various functions. One member controls satisfaction levels while another member controls marital bliss.

Satisfaction level controlled by a gene?
We found that this single, collaborative article published in the Journal of Neuroscience answered our question the best, given today’s technological knowledge and funding set aside for the pursuit of a happy society. The article, “Genes, Economics and Happiness” studied the feeling of subjective well being in twins in a genetic association study. Studying twins makes sense because scientific studies require a “control”, with which they can compare any differences, such as environment and economics, all other factors being equal. Who can be a better control than a person’s own twin? Let’s find what these scientists collaborating between four universities in three countries summarized. Subjects were asked questions like, “How satisfied are you with your life as a whole?”

1. About 33% of life’s satisfaction can be explained by genetic variation – you inherit your family’s feelings of satisfaction.
2. There are molecular genetic associations with subjective well being – meaning that although previous studies have shown that there is a baseline happiness that is inherited from family, certain experiences can interfere with that baseline. An indirect molecular effect of life’s stressful events?
3. As an example, they studied in detail the Serotonin Transporter gene (5-HTTLPR, also named SLC6A4), or SERT a key brain protein it encodes. Serotonin is a chemical released by one neuron and received by another neuron. The protein has a longer form and a shorter form. Initial findings suggested that families that inherited the longer form were more satisfied. But this study produced mixed results, implying that certain experiences can interfere with the length of this gene. The 5-HTT gene has been studied for over 20 years. This gene encodes a protein (located on the cell surface membrane) that absorbs serotonin into the neuron in parts of the brain that influences mental states.
4. Heritability of happiness rises as people age. At different points in life’s course genes and environment play a different role.
5. In particular, gender does not systematically effect happiness.
6. There are other genes with functions involved in gene-environment interactions and satisfaction.

This study encourages economists to consider biological differences in their studies. Economists are interested in the impact of income or unemployment on feelings of satisfaction. Psychologists describe a “set point” or “happiness levels” that exist in families. Since, optimism is linked in families carrying a more efficient version of the 5-HTT gene, all of us are interested.

Wedded bliss gene?

Dr Claudia Haase, Northwestern University says couples with the 5-HTTLPR gene were most happy in their marriages

There is recent evidence for a wedded bliss gene. Scientists have long observed that married people are generally happier than divorced people. Couples with the 5-HTTLPR gene were most happy in their marriages. Couples with two shorter forms of this gene are likelier to be happier in a compatible relationship rather than suffer in a bad one. Emotion is an important element in marital bliss. The marriage thrives under certain emotional levels. People who inherit the two longer forms of this gene respond less to emotional levels in marriage. Read, “Claudia Haase’s New Study links DNA Marital Happiness“.

Can we be re-engineered biologically to be happier?
If we do have this satisfaction gene and we find that some of us do not have this happiness gene, then what? Will it be allowed by FDA to walk into a clinic to get diagnosed “for a happiness gene” and then get a bioengineered happiness gene if the doc says we lack one? Will insurance pay for such a happiness – gene – bioengineering therapy? What will it’s medical code termininology read like? Will insurance pay for “diagnosing a SNP or marker” that causes change in the “happiness gene” in an unhappy individual?

Pursue Natural felt it could begin by searching for any peer – reviewed published work on happiness genes. Peer – reviewed would indicate that fellow scientists respect the methodology or scientific thoroughness with which this scientist approached the issue of discovering the happiness gene.  We discussed above our findings. What are your opinions on the happiness gene? . Can you imagine the impact of an eternally happy society?

Other Authors who have recently discussed the Happiness factor
Happiness from having a purpose in life linked with gene activity
Your happiness type matters
Happiness can affect your genes
Looking to genes for the secret to happiness
Wedded bliss or blues? Scientists link DNA to marital satisfaction

The first Phenome Center established to research interactions between genes and the environment

Certain people become more susceptible to environmental toxins and food allergens than other people exposed to the very same factors. Why is that? How are some people completely healthy even after they eat food that makes other people very sick? Why are some children in the autistic spectrum disorder growing up in the same environment and eating the same food as their healthy neighbors children?

To research the answers to these growing questions in an increasingly post – industrial modern society used to extremely convenient modes of transportation and fast food, a large scale multi-disciplinary approach is required.  Joining together in this effort are  the MRC-NIHR Phenome Centre, which opened recently in the United Kingdom, with a collaboration between Imperial College London, King’s College London and analytical technology companies Waters Corporation and Bruker Biospin.

The center has ten million pounds of funding for the first five years. However, if you wish to support such relevant research do not hesitate to contact the institute. Studying the phenome will help determine how diet, lifestyle, the environment and genes combine to affect biochemical processes that lead to disease.

Professor Frank Kelly, co-investigator at the Centre and director of Analytical and Environmental Sciences Division at King’s College London, said, “This technology is already in use in medical research but only on a small-scale. With the creation of this new facility, it will now be possible to get a complete and accurate biological read-out of thousands of individuals.” Reported in  Pharmabiz, June 13, 2013. Instruments of the highest degree of sophistication will detect the different types of bacteria naturally occurring in the gut, which can influence our health. Read this previous article on how hook worms can cure multiple sclerosis in some patients or this previous link on “the worm theory and how it could strengthen the immune system”.

The Centre will also include a state-of-the-art international training facility. There are no limits to the breakthroughs in health we might see as a result of this visionary, large data work approach at the NIHR-MRC Phenome Centre.

The 2013 winners announced for the Breakthrough Prize in Lifesciences

“A high-profile, spectacular recognition,” says Marc Tessier-Lavigne, the Rockefeller University’s president.

Dr Cori Bergmann, of Rockefeller University

Dr Cori Bergmann

Scientist recipient #1 researches the role of genes in brain connections (neural circuits) and what effects them. Genes in the brain control behavior and function by receiving a signal and acting on this information via a fixed pathway. This scientist’s work has identified sensory inputs, genes which respond to them through their fixed pathways and hence, how sensory inputs control or regulate such genes.

Dr Titia de Lange, of Rockefeller University

Dr. Titia De Lange

Scientist recipient #2 researches what detects and repairs DNA and prevents cancer (telomeres and shelterin complex). The telomere complex repairs damage to the body from dangerous elements. Early in cancer development, telomere function gets erroded. This scientist’s work clarified how the loss of the telomere-shelterin complex function can drive cancer forward.

The Breakthrough Prize in Life Sciences Foundation

Administers the Three million dollar annual Breakthrough Prize in Life Sciences, which recognizes excellence in research aimed at curing intractable diseases and extended human life. the prize is founded by Art Levinson, chairman of the board of Apple and former CEO of Genentech; Sergey Brin, co-founder of Google Inc.; Anne Wojcicki, co-founder of 23andMe; Mark Zuckerberg, founder and CEO of Facebook, and his wife Pricilla Chan; and Yuri Milner, founder of the Russian internet company Mail.ru.

What does this prize mean for you?
This prize assures you that you and your loved ones are not suffering alone in cancer and brain/behavior malfunctions. There are dedicated scientists, working diligently, step-by-step to discover the marvellous mystery of how the living thing lives, breathes, thinks, behaves, malfunctions, gets sick, and responds to environmental toxins like pesticides, herbicides, or food toxins like high fructose corn syrup or metal toxins like lead. Most scientists work simply for the joy of discovery. They work long hours, late into the night for very little pay. Many of you might even laugh at them calling them names like “gheto dwellers” because many brains arrive from foreign countries and dry their clothes on clothes lines to save money instead of using the dryer in the laundromat. Others might laugh at them because these scientists cannot afford cars in large college campuses and walk miles to pick up their weekly groceries. Yet, they work with happiness, and courage.

Many of you have chosen not to take science courses in college and therefore, do not understand how marvellous the mystery of the complex cellular organism is. When you are on funding agencies, you simply cannot understand why an experiment might take years to show results. You might even poke fun at these “lazy, poor, gheto nerds”. You might be reminded that a typical cell under research has a life cycle of several hours to several days, with embryo and stem cell study cell life cycles taking several months.

This prize assures you that people who are capable of judging the progress of science are keeping you infomred. This prize assures you that dedicated people are taking care of you, actually excellent care of you, even though you might not even have the time to stop and contact them and show your appreciation. This prize assures you that a scientist you appreciate is being rewarded with a lot of money, long deserved – probably far better deserved than many other fields of work that contribute nothing, produce nothing and yet, are capable of great destruction.

What you can do

This prize assures you that you are taken care of. Perhaps, you can take charge and create more such foundations that reward long-term, pain-staking scientific enquiry in your community scientists, in your local university; hard working people whom you might have ignored and called “poor” and who might not get recognized internationally but are contributing daily, and happily.

Could the cure for cancer be a simple master switch solution by a Massachusetts based company?

Yes, blocking of a few master genetic switches associated with “super enhancers” might be a simple cure for cancer, says Dr. Richard Young, of Whitehead research institute, MA, senior author in two papers in the prestigious, peer – reviewed paper, Cell, and founder of a start-up company, Syros Pharmaceuticals, with the goal to cure cancer. The company has raised 30 million dollars to support its goal to cure cancer by finding and switching off the master switches in each type of cancer. You may click here to read the Cell paper led by Dr. Jakob Loven, for “Selective inhibition of tumor oncogenes by disruption of super enhancers”, and here to read the Cell paper led by Dr. Warren A. Whyte, for “Master transcription factors and mediator establish super enhancers at key cell identity genes.  Both the papers have a single, master illustration explaining the main concept. It is must see to understand how simple the hypothesized solution is.

Dr Young’s team says a normal cell regulation is remarkably less complex, with core genes controlled by only a few hundred super enhancers. With this hypothesis, cancer research focus is forever changed since April 2013, and gives remarkable insight to how a single fertilized egg from a father and mother can develop into a unique individual, with two-thirds of his/her diseases having a genetic determination. Loss of old super enhancers and assembling a cluster of new enhancers drives cell identity as a human grows develops.

For years cancer scientists have been reporting their discoveries of the mediators responsible for over expression of cancer genes. What makes Dr Young’s work more unique is that it suggests that a few master switches might control this gene at super enhancer regions. There are thousands of cancer gene transcription factors in the literature. One example is the study of pancreatic cancer, the fourth commenest cause of cancer related deaths in the western hemisphere. Several key genes have been shown to play a role in pancreatic cancer, including the oncogene K-RAS and several tumor suppresor genes including some from the TGF signalling pathway. The researchers discovered that the Fibroblast growth factor receptor gene 4 (FGFR4) was overexpressed in almost two-thirds of pancreatic cancers. They found a research outside this gene called intron 1, was greatly extended in pancreatic cancer cells. Two sites binding transcripton factors and two sites binding mediators were identified, and additionally, the team discovered which mediator was essential for over expression of FGFR4 to cause pancreatic cancer. You may read about this pancreatic cancer work led by Dr. Helen C Hurst of London by clicking here. Might this deadly pancreatic cancer too be controlled by inhibiting one or more of the several hundred master switches?

Do you prefer a non scientific explanation of the above solution? A very simple explanation of the complex work done by Dr. Richard Young and his team of enthusiastic young scientists is given by Amy Maxmen in the respected weekly journal, Nature and you might read it by clicking here. She appropriately titles it “Super-powered switches may decide cell fate”. Different cells in the body have the same genes swithced on at different times. When such cells are switched on by a super enhancer complex due to unknown factors (as yet), then the cell becomes cancerous. You might say that cancer cells are “fueled” by “super enhancers”, and might suggest inhibiting such a fueling source to cure cancer and you might be correct to be hopeful, albeit with a heavy dose of patience. Last year it was discovered there are a million enhancers in the human genome. Dr Young speculates that some of these enhancers act together in large clusters and function as a unit. How are cancer cells able to employ such super enhancers to produce more of their harmful factors that lead to aggressive tumors? 

Dr. Richard Young and his team of enthusiastic young scientists deserve to know if you support their goal. Do write to them if you do to encourage them. Scientists work long hours tied to a laboratory bench. Although they love their job to solve mighty goals, receiving your notes of encouragement will inspire them further. Do keep in mind that discovery through clinical trials with FDA approval to doctors office may take a decade or longer and might cost a billion dollars for each drug in research over that period. So 30 million dollars will not take them too far without your support and creative solutions to funding.
Email: Dr Richard A. Young and his team at young@wi.mit.edu
Snail mail: Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA

Why the same drug acts differently in two people: how your NAT2 genes dictate the drug’s action in your body

Two people are in pain. Both of you take the same drug; one of you feels in less pain faster than the other. How? Why? The answer, that your genes may be different is making the drug manufacturers wonder if they can take better care of your health by first requesting a genetic test. Could it be, that a drug might be personalized to work just for your genes? Sure, say most drug manufacturers. The advantage would be that there would be fewer bad reactions from two people taking the same drug with exactly similar prescriptions, but with one person showing side reactions, while the other is simply fine.

Personalized Medicine
Many factors control why you respond differently to the same drug from another person. One is the gene factor. Allow me to enlarge upon a single gene called NAT2. I choose this gene because it is my favorite gene. It explains so much so simply. When a drug company develops a drug through clinical trials it tries to judge dosage by weight and height and more complex formulae. None, however, take into account that the genes may have subtle differences, although the drug companies may have researched and stored this data. Today, a drug company sells one drug to all people. Soon the day is coming when the drug company will ask you, “How do you want your drug?” Well, not exactly that phrase. They will test your genes, figure out what your body can tolerate and then calculate a dose close to what you should be able to tolerate.

Here’s how one gene controls your body’s drug reaction
Genetic variability in the NAT2 gene has long been recognized to be the cause of differential ability to metabolize a variety of medicinal drugs. The NAT2 gene produces an enzyme mainly in the intestine and liver. It detoxifies through arylhydrazine compounds. NAT2 gene produces important enzymes that breakdown drugs for major diseases like tuberculosis. Some people have a variation of the NAT2 gene that may make them more susceptible to bladder cancer. Which means that if you have a different variation of the gene you may rest assured you may never get bladder cancer, no matter what you eat or which water you wade into.

International anthropologists have gathered vast amounts of genetic data from various world populations (click hereto read). It shows that if your ancestors were hunter – gatherers then, your NAT2 gene was different than if your ancestors were agricultural – pastoral.

The NAT2 gene will control your destiny.  Soon, perhaps, NAT2 gene will be a household word, discussed just like your high blood pressure or baldness in the family. Either you have the NAT2 gene that is a drug manufacturer’s dream, or can never have bladder cancer, or have to have a personalized drug manufactured for your ability to breakdown the drug for your disease. You will care to know more about this gene. NAT2 is already working inside you. Are you working for your own NAT2 or your neighbor’s NAT2 is the question?

Abstract

Expression of novel genes in response to various stimuli in the human dermatophyte Trichophyton rubrum

Background

Cutaneous mycoses are common human infections among healthy and immunocompromised hosts, and the anthropophilic fungus Trichophyton rubrum is the most prevalent microorganism isolated from such clinical cases worldwide. The aim of this study was to determine the transcriptional profile of T. rubrum exposed to various stimuli in order to obtain insights into the responses of this pathogen to different environmental challenges. Therefore, we generated an expressed sequence tag (EST) collection by constructing one cDNA library and nine suppression subtractive hybridization libraries.

Results

The 1388 unigenes identified in this study were functionally classified based on the Munich Information Center for Protein Sequences (MIPS) categories. The identified proteins were involved in transcriptional regulation, cellular defense and stress, protein degradation, signaling, transport, and secretion, among other functions. Analysis of these unigenes revealed 575 T. rubrum sequences that had not been previously deposited in public databases.

Conclusion

In this study, we identified novel T. rubrum genes that will be useful for ORF prediction in genome sequencing and facilitating functional genome analysis. Annotation of these expressed genes revealed metabolic adaptations of T. rubrum to carbon sources, ambient pH shifts, and various antifungal drugs used in medical practice. Furthermore, challenging T. rubrum with cytotoxic drugs and ambient pH shifts extended our understanding of the molecular events possibly involved in the infectious process and resistance to antifungal drugs.

Background

Trichophyton rubrum is a cosmopolitan dermatophyte that colonizes human skin and nails and is the most prevalent cause of human dermatophytoses [1,2]. During the initial stages of the infection, dermatophytes induce the expression of adhesins and unspecific proteases and keratinases that have optimum activity at acidic pH values [3], which is probably because the human skin has an acidic pH value [4]. The secretion of these proteases, which have been identified as an important step in fungal pathogenicity and virulence [5,6], act on keratinous and nonkeratinous substrates to release peptides that are further hydrolyzed to amino acids by putative peptidases. The metabolism of some amino acids shifts the extracellular pH from acidic to alkaline values at which most known keratinolytic proteases have optimal enzymatic activity[7–9]. T. rubrum also responds to the environmental pH by altering its gene expression profile[9,10].

Molecular studies have been performed with human pathogens such as Candida albicans,Histoplasma capsulatum, and Paracoccidioides brasiliensis, and the results thus obtained have helped to determine the fungal transcriptional profile and characterize the genes involved in host-pathogen interactions and environmental stress responses [11–13]. Previously, a collection of T. rubrum expressed sequence tags (ESTs) was obtained from distinct developmental phases[14,15]. However, determining the transcriptional profiles in response to different cell stimuli is necessary for extending our understanding of diverse cellular events, and the results from such studies may reveal new signal transduction networks and the activation of specific metabolic pathways. Functional analysis of the genes involved in these molecular events will help in evaluating their roles as putative cellular targets in the development of new antifungal agents.

Our study aimed to extend the T. rubrum genomic database by adding expressed gene resources that cover different aspects of cellular metabolism. Moreover, the data can help to generate useful information to screen valuable genes for functional and postgenomic analyses. The EST collection described here revealed the metabolic adaptations of the human pathogen T. rubrum to changes in the ambient pH and carbon sources and also provided information on the adaptive responses to several cytotoxic drugs. 

__________________________________________________________________________________

Transcriptional profiling reveals the expression of novel genes in response to various stimuli in the human dermatophyte Trichophyton rubrum

Nalu TA Peres¹, Pablo R Sanches¹, Juliana P Falcão^1,3, Henrique CS Silveira¹, Fernanda G Paião¹, Fernanda CA Maranhão¹, Diana E Gras¹, Fernando Segato¹, Rodrigo A Cazzaniga¹,Mendelson Mazucato¹, Jeny R Cursino-Santos¹, Roseli Aquino-Ferreira¹, Antonio Rossi²and Nilce M Martinez-Rossi^1*

• *Corresponding author: Nilce M Martinez-Rossi nmmrossi@usp.br

Author Affiliations

¹Departamento de Genética, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto 14049-900, SP, Brazil

²Departamento de Bioquímica e Imunologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto 14049-900, SP, Brazil

³Current address: Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, 14040-903, Ribeirão Preto, SP, Brazil

For all author emails, please log on.

 

 

 

 

BMC Microbiology 2010, 10:39 doi:10.1186/1471-2180-10-39

 

The electronic version of this article is the complete one and can be found online at:http://www.biomedcentral.com/1471-2180/10/39

Is sleep overrated or is the “Executive nap” highly recommended for multiple sclerosis, rheumatoid arthritis and crohn’s disease??

Essential immune system gene reacts to infections controlled by the body’s circadian clock genes. From breast cancer to rheumatoid arthritis, there appears to be a connection with the daily rhythm of a living being today. Read the journal links below to learn about the research yourself. My suggestions would be to get a good nights sleep. Switch off all lights for an undisrupted number of hours. Cover all light emitting gadjets like cell phones, blinking laptop lights and more, and make a natural dark environment to sleep “like a baby”.

Nap Nanny makes it easy for babies to sleep anywhere, anytime. What about you?

Also, steal quick, short nap times like a tycoon – called Executive nap, during the day.

Jack Welch advises on winning. Did he nap? Did he get a good night's sleep? He was CEO of GE.

1) Dr Richard Steven in the journal Epidemiology (2005) says that in breast cancer, something in modern life is the culprit. Light during the night of sufficient intensity can disrupt circadian rythms, which may be particularly harmful during key developmental stages.

2) Dr Giovata Cavadini and colleagues surmised in the journal, Proceedings of Natural Academy of Science (2007), that the inflammatory clock gene response may by inducing fatigue, decrease the quality of life in autoimmune disease. The regulation of sleep depends on a self-sustained circadian pacemaker, which includes a molecular mechanism which involves the clock genes. It is still debated if sleep changes the course of infection. In multiple sclerosis, rheumatoid arthritis and crohn’s disease both fatigue and increased TNF-alpha has been described. In infectious diseases, TNF-alpha serves to eliminate the agent of disease.

Related Articles:
Multiple sclerosis cured by worms?

Autistic child and multiple sclerosis parent – a connection?

National TV news PBS asks why is Autism rising in six video series.
 

Our genes respond differently to our diets

How do our genes respond to our diet?

Researchers studied cholesterol genes in six generations of baboons and found that siblings may have totally different reactions to the same high-fat diet and identified 53 possible genes for regulating HDL, which is one of the traits associated with an increased risk of heart and blood vessel disease. These researchers are looking further into these pedigreed, baboon families on the same fatty diet but with different levels of HDL and LDL.

Baboon and human HDL genes, in particular, are very similar and on the same chromosome making such research very meaningful for Genetics researchers at the Southwest Center for Biomedical Research (Texas). The chief researcher, Dr. Laura Cox was inspired as a child to understand the basic biology of all living things. As a society, we owe Dr. Cox and her team, special thanks to the tremendous progress in medical research in the field of diet and heart disease. Her team has shown significant correlation between genes and circulating fat, glucose, body weight and diabetes related symptoms (Heredity, 2008).

If heart disease research is important to you, do send a note to your favorite scientists and encourage them.