This article first appeared in the August 2014 issue of Complete Wellbeing magazine

Sleep By Ratan Singh

Taming the [body] clock

Midnight conference calls, unavoidable deadlines, late-night parties—just gulp some coffee or an energy drink and we’re good to go. But in our hurry to do everything, we lose out on something valuable
By Ratan Singh

Our sleep requirement changes throughout the different stages of our life, depending on our physical and mental health, lifestyle and work pressure.
Today, we are constantly being stimulated with technology and various modes of entertainment, in addition to juggling the unceasing pressures of work and home. Everybody seems to need more than 24 hours in a day to carry out all their activities. Shortage of time has become a mass epidemic affecting all sections of society—school-going children, college students, working professionals and stay-at-home mothers.

So where can we get hold of extra time?
Since we can’t ‘buy’ time, we tend cut down spending hours on those activities we deem ‘unnecessary’. For most people, this unnecessary activity happens to be—you guessed it—sleep. Devoting a quarter of our 24 hours every day has become too precious for most of us. So we end up compromising our slumber.
However, let us imagine the ideal scenario where we have enough time in our lives to do all the activities we want. The question that arises then is, “How many hours should we sleep?”

Optimal sleep duration experiment
A study was conducted to find out the answer to this commonly-asked question. Simulating the lifestyle of ancient cavemen, volunteers entered a sleep lab every evening by 6 pm and left the lab by sunrise. The inside of the lab had been darkened completely and made sound-proof. The volunteers’ sleep was monitored and their eye movements were recorded to measure how much time they slept and the quality of their sleep. Also, there were no other activities that the volunteers could indulge in.

The result
Initially, to recover their accumulated ‘sleep debt’, they did sleep for 10 – 12 hours; but the following nights all of them slept for an average of seven hours and 45 minutes with a variation range of seven to eight hours. Surprisingly, the volunteers were in a happy state of mind during the entire experiment.
Across cultures and geographic regions the sleep hours are fairly similar, averaging about seven to eight hours. And this holds true even for the Norwegians living in the Arctic Circle where they experience extended durations of daylight and night-time.

The affect of mental and physical health on our sleep
Our sleep duration also varies according to our health status. For example, a person with a mental illness such as schizophrenia has a reversed cycle of sleep and wakefulness, with the person sleeping only during the daytime. A person with hypothyroidism has an enhanced sleep requirement; such a person is inclined to sleep at anytime, even if they’ve had a restful sleep of eight hours at night.

How to measure your sleep debt
Sleep debt is related to ‘sleep latency’—which is the stretch of time between going to bed and falling asleep. This implies that the more sleep debt you accumulate over the week, the less time you will need to fall asleep. It is a simple test you can perform—just lie down and close your eyes for 20 minutes. If you don’t fall asleep during these 20 minutes, then your sleep debt is zero. This indicates that you have been sleeping enough. Note: this test of sleep debt presupposes that your inability to sleep is not due to pain or illness.
There is also a downside of having zero sleep debt, because it signifies that you will have a hard time in falling asleep. In other words, you need to build up some sleep debt, it should be just enough to be able to initiate sleep within a reasonable time-frame and maintain a moderate range of ‘sleep latency’.

Restoring the sleep debt
Most people would have built up a sleep debt, either by studying through the night, working long hours or by various other ways.
Does that then mean that once we start a sleep debt, we go on accruing it? No, you can restore your sleep debt accumulated during the week. This is done with planned naps. You should make the time to sit or lie down quietly for 20 minutes or more, two to three times during the day.
What is important in this ‘pay back’ of sleep debt is the duration of your naps. It must consist of several minutes; not the catnaps of one or two minutes that you get in a meeting, conference or lecture hall because of your high sleep debt. This method of renewing your sleep debt was proved in an extreme experiment.

Sleep ‘pay back’ experiment
The volunteers in this experiment were awakened every minute during their regular night sleep. They did fall back to sleep immediately within 10 – 15 seconds and they completed their eight hours of sleep. However, because of the repeated interruptions, the volunteers were sleepy and irritable the next day.
They tried to offset these symptoms by having short naps of 10 – 15 minutes. But towards the end of the day a new debt accrued and the sleep debt symptoms showed more intensely. This experiment shows that our ‘sleep bank’ doesn’t accept small piecemeal credits. We need sustained sleep of at least 20 minutes to partially offset our sleep debt.

Can you make up for lost sleep on the weekend?
Suppose you can afford only six hours of daily sleep during your working five-day week; you are therefore carrying a sleep debt of 10 hours during the week, given that you need eight hours of sleep every night. Thus, every night through the working week you continue to incur two hours of sleep debt. However, sleeping late on weekends and holidays will not help, because you have to balance your sleep debit with a credit of 10 hours of sleep. Also, this effect or recovery will be transient because your body clock will not allow you to sleep for long; your body will stop secreting the sleep hormone melatonin. And new sleep debt will begin to accumulate.

What is the way out then?
My solution to this problem of continually accumulating sleep debt is to have a regular sleep of about seven-and-half hours at night, followed by two or three bouts of 20-minute naps during the day. In this way, you can even anticipate a sleep debt coming your way.
If you have an upcoming party or conference call that you have to attend late at night, you can take preventative naps. But it is important to not make it a habit or you will end up with ‘sleep reversal’. You will find yourself dozing off in the daytime or going about your work in a drowsy state because of your reversed mind/body circadian rhythm.
So take care of your sleep debt and stay alert and happy.

Symptoms of
sleep debt
>> Drowsiness and laziness during daytime
>> Fatigue
>> Irritability
>> Vague body aches
>> Decreased or absent sex drive
>> Brain fog and lack of focus
>> Accident prone
>> Lack of initiative
>> Habitual procrastination
>> Low energy

The sleep debt reference values
This is the time it takes you to fall asleep and how that correlates to your sleep debt:
0 to 5 minutes: High sleep debt—you are in danger and may be prone to accidents and illnesses
5 to 10 minutes: Borderline
10 to 15 minutes: Manageable sleep load
15 to 20 minutes: Full alertness

Ratan Singh is a Consultant in nutritional and neurobehavioural psychology, Jaipur Hospital, India.

Posted in Uncategorized | Tagged , , , | Leave a comment

Chess and brain and Vishy Anand
The first Indian grandmaster Pravin Thimpsay as quoted by in The Times of India Times Sport, November 8, 2014, feels that the challenger Vishy Anand wouldn’t be able to sustain his peak performance in a long game say beyond 40 moves. Given Vishy’s age over the defending champion Carlsen, such an opinion is understable. But I feel Vishy can compensate for age with more practice and meditation and relevant nutrition. It seems to me that Vishy’s cellular glucose and/or oxygen uptake in brain starts to dwindle after say the “40 moves”. His task should be to maintain a steady level of blood glucose and oxygen levels. He should insist upon good ventilation, and no odors around that may cause a reaction in brain. Glucose level is intertwined with insulin release. There are supplements and diet to maintain a steady insulin release. A hypoglycemic condition must be warded off during the chess game. Care should be taken to avoid Type 3 diabetes. Vitamin B12 level in the brain—not just in blood—should be maintained at 1000 pg/mL.

Posted in Uncategorized | Tagged , , | Leave a comment

A twist in the GFCF diet

I recently learnt the following that is exciting and so can’t resist sharing.

#1. Gluten is just one issue, there may be other issues too, hidden in grains—not just in the familiar wheat, rye, barley, oats. So we must stop all grains. Context here is of course the “GFCF” diet so very popular among the ASD circles.

#2. And this one is a pathbreaker: A fungus called Secale Cornicum (in homeopathy), also called “Black Smut” —an ergot—infects wheat and rye. So this fungus may be the real culprit rather than gluten.

I used to have severe pain in inguinal region and lower back (Lumbago pain) lasting for days and forcing me to lie down for 10 minutes often. At last when it got unbearable and obstructing me from my hospital duties, I bought Secale Cornicum in 1/30, 1/200 and 1/1000 dilutions (homeopaths will call them 30X, 200X and 1000X or potencies). I kept them ready. My plan was to start with 1/30, wait for 10 minutes and, if no relief, to next try 1/200 and so on. Did I say “10 minutes”? Lo and behold I took the 1/30 dilution two to three drops sublingual and —hold your breath—within a minute the severe pains of inguinal region and lower back that were crippling me past four days just melted away. Couldn’t believe but it was right there. I now continue taking it as a preventative measure. Placebo effect? Well I don’t care. In any case friends its true that the ergot does infect grains. So, talking in the mainstream language, we must do anti-fungal treatment—only I did the same but the homeopathic way.


Posted in Uncategorized | Leave a comment

19-year boy speaks “Mummy” first time, mother shocked

This was a boy of age 19 and mentally subnormal and ASD. Never spoke a word except long ago when he used to blurt out “Papa” but that too he stopped. He could sing tunes of songs but not words. Somewhere I had read of DMG. And it hit. I gave him the full methylation cycle formula, DMG, folinic acid and mB12. The sister, who had given up her job to be her brother’s full time care giver, reported as follows.

“It was a marriage ceremony. We decided to take him along. There the mother was standing far from him and he was near his maternal uncle (“Mama”) who is confined to wheal chair. Suddenly the boy/brother shouted “Mummy Ao” (in english its “Mummy come”)”. The sister continued: “The mother was shocked. All were very happy. He went on verbally teasing his “Mama” and “Mami” (wife of maternal uncle).”

So, just imagine the state of the mother who was hearing “Mummy” from a 19-year boy first time ever. Shocked and scared (a ghost had entered her son?).

In retrospect I think its the dose of DMG. The sister had asked me once if she could increase the dose as she was noticing sounds of some vaguely formed words in her brother to which I had replied “Yes of course”.

The dosing I believe is unique to the patient and point in time. There are many paths of action ascribed to DMG. For example, it increases the oxygen supply to brain, participatel in the methylation cycle.


Posted in Uncategorized | Leave a comment

De-link suicide and Depression

My Letter has been published in the recent issue of Nutrition & Mental Health, the Quarterly Newsletter of the International Schizophrenia Foundation, Winter 2014, page #2. Its titled De-linking Suicide and Depression. As I don’t know how to upload the entire Newsletter, I “copy and paste” just my Letter here below. I propose that suicide can’t be predicted by depression alone. I also propose that its wrong or rather counter-productive to treat suicidal tendency (para-suicide) with anti-depressants, particularly the SSRIs. Further, I propose a new line of treatment. Please read below.

De-linking Suicide and Depression
The N&MH of Autumn 2013
carries two separate but linkable items,
which together can explain a lot about
suicide and perhaps the school shooting
instances of homicide and suicide.
The first item, in MindCheck, discusses
selective reuptake inhibitors, all of
which indirectly cause down-regulation of
the neurotransmitters, which is the body’s
endogenous feedback response. It seems
paradoxical that anti-depressants aimed to
decrease depression and, by implication,
suicidal ideation, end up promoting it
but this is what happens. Drug companies
either don’t bother about the biological
feedback loops or don’t do drug trials lasting
more than six months. The feedback
loops altered by external factors like the
anti-depressants may take time to kick
in and manifest in the form of increased
suicidal ideation. In treating depression,
psychiatry today may simultaneously
increase the incidence of suicidal ideation
and, perhaps, homicide, resulting in school
shootings. Most of the perpetrators in these
shootings have been on anti-depressants.
The second item (In Brief) de-links
suicidal ideation and depression. Clinically,
suicide is not a sine qua non of depression
alone; suicide is also possible in schizophrenia.
Suicidal ideation has been linked with brain
inflammation more than with depression.1
Given this finding, why use antidepressants
at all? With any suspicion of
suicidal inclination, the target of treatment
should be brain inflammation rather than
depression, because the anti-depressants
may decrease the body’s endogenous
production of neuro-transmitters and exacerbate
suicidal ideation as evidenced in
those involved in school shootings. Brain
inflammation can be easily detected
radiologically and by blood markers like
C-Reactive Protein and homocysteine.
There are medicines used by neurologists
who often deal with inflammation caused
by traumatic head injury and other neurological
conditions. Good orthomolecular
therapeutic agents free of side effects are
omega-3 and GLA and the homocysteine
lowering protocol.
With suicidal ideation and depression,
the first target should be suicidal
ideation and treatment should be aimed
at lowering inflammation. Suicide, after
all, is the only emergency condition in
psychiatry and therefore should be attended
on a priority basis.
1. Depression and Anxiety, 2013; 30/4: 307-314.
–Ratan Singh, PhD
Member, ISOM (International Society of Orthomolecular Medicine)
Consultant in Nutritional and
Neurobehavioural Psychology,
Jaipur Hospital, Jaipur, India.


Posted in Uncategorized | Leave a comment


Recently I am getting good response in depression cases who have been on anti-depressants without benefit for four and seven and more years. Their depression got relieved in a maximum of seven days. The beauty is that the patients do with diet what I teach them and they on their own discover the cause in their individual case. They are happy with my approach of manipulation of diet. They get a tool in their hands. In reply to the objection that the same may not be true in other cases of depression, these patients shoot back: “I am concerned with my condition only. I now know what makes me depressed. I need no other proof.”
But if the patient is in doubt (initially), then I ask her/him to repeat the diet experiment until (s)he is convinced with the cause. And this is what they do. Among the three patients I mention here, one is owner of a big busy hospital in a prominent city. He was on anti-depressants for over seven years.

Posted in Uncategorized | Tagged , , | Leave a comment

Correspondence on Causes & Treatments of Schizophrenia

Dear readers:

I don’t know how to upload a PDF file to my web site. This PDF file is my Correspondence on causes and orthomolecular treatments of schizophrenia published in the Journal of Orthomolecular Medicine, 2012, vol. 27, No.4.  I have just “copy-pasted” it below with kind permission of the Editor of this journal, published from Canada. So keep reading below. Please note that the references are all the way down on the “second page”, the page # 199.

Ratan Singh, Ph.D., 91-141-4022609,,

Journal of Orthomolecular Medicine, 2012, vol. 27, No. 4.

p. 198, Journal of Orthomolecular Medicine Vol 27, No 4, 2012

The Adrenochrome Hypothesis

Differences arose between Sen and Prousky on the validity of Hoffer’s adrenochrome hypothesis of schizophrenia.1,2 Two points are noteworthy in this context:
1. Hoffer himself called adrenochrome a “hypothesis” although he concluded that the adrenochrome hypothesis was the best fit hypothesis among other competing hypotheses of the schizophrenia syndrome.3
2. We should not overlook the fact that schizophrenia is really schizophrenias (plural). For example pellagra, still around in many parts of the world, may be mislabeled as schizophrenia. Similarly, cerebral allergic reactions to gluten (gluteomorphin) can give rise to clinical features that would be indistinguishable from schizophrenia, and therefore would be overlooked by most psychiatrists.
Hoffer himself sometimes moved away from the adrenochrome hypothesis. For example, he advised us to think of alternate treatments (i.e., hypotheses) if a patient had not responded to therapeutic doses of niacin. Hoffer considered hypothyroidism as a possible cause of schizophrenia.4 He even quoted a study by Danziger that showed recoveries in 80 schizophrenic patients that were administered natural desiccated thyroid for at least 100 days, and who were ill for six months or less.5
Foster,6 Pataracchia,7,8 Campbell-McBride,9 and others have summarized the alternate causes or hypotheses of schizophrenia, such as subclinical hypothyroidism, cerebral allergy to gluten, sugar and petro chemical inhalants, heavy metal toxicity, and candida/gut dysbiosis. In any individual case, any combination of causes might be implicated in the genesis of the schizophrenia syndrome.
Although, at least to my knowledge, adrenochrome has not been measured and compared between schizophrenic, non-schizophrenic and normal control groups of population, we can draw conclusions in favour of niacin and hence, indirectly for the adrenochrome hypothesis, from Hoffer’s studies and reports that spanned many decades. Outside of Hoffer, there have been publications giving indirect credence to the adrenochrome hypothesis. For example, Wittenborn published data demonstrating that acute-onset patients (ill for six months or less) were having intact inter-personal relations as a result of niacin treatment.10
Hoffer’s writings also stressed the value of psychosocial factors when he talked of food, shelter, and respect as critically valuable factors in recovery without psychiatric drugs.11 In the case of chronic schizophrenic patients, who are likely to develop negative symptoms, much like the well known symptoms of “institutionalization or hospitalization syndrome,” the useful hypothesis may be something other than the adrenochrome hypothesis. There is even evidence of gluten sensitivity in chronic schizophrenic patients. They may have become chronic because the treating physician didn’t consider gluten as a hypothesis of schizophrenia. A 2009 publication described a lifelong schizophrenic patient that recovered following a gluten-free, low-carbohydrate ketogenic diet.12
This leads to another point raised in the Sen and Prousky correspondence. Prousky argues in favour of integration and some kind of cooperation between orthomolecular and orthodox mainstream medicine. If orthomolecular medicine is integrated with the mainstream, then the former will lose its identity and vitamins will become available on “physician’s prescription only.” The public at large will lose the right to use vitamins as food supplements and the cost of health maintenance will become unaffordable. Let both streams of medicine grow, thereby giving people the right to choose the therapy they want.
–Ratan Singh, PhD
Consultant in Nutritional and Neuro-
behavioural Psychology
Jaipur Hospital, India

Correspondence                                                                                                                  199

1. Sen DR: Does vitamin B3 really reduce adrenochrome? J Orthomol Med, 2012;27:93.
2. Prousky JE: Does vitamin B3 really reduce adrenochrome? Author responds. J Orthomol Med, 2012; 27: 93-94.
3. Hoffer A: The adrenochrome hypothesis of schizophrenia revisited. J Orthomol Med, 2009; 24: 160-182.
4. Hoffer A: Thyroid and schizophrenia. J Orthomol Med, 2001; 16: 205-212
5. Danziger L: Thyroid therapy of schizophrenia. Dis Nerv Syst, 1958; 19: 373-378.
6. Foster HD: What Really Causes Schizophrenia. Victoria, BC. Trafford Publishing. 2003.
7. Pataracchia RJ: Orthomolecular treatment for schizophrenia: a review (part 1). J Orthomol Med, 2008; 23: 21-28.
8. Pataracchia RJ: Orthomolecular treatment for schizophrenia: a review (part 2). J Orthomol Med, 2008; 23: 95-105.
9. Campbell-McBride N: Gut and psychology syndrome. J Orthomol Med, 2008; 23: 90-94.
10. Wittenborn JR: A search for responders to niacin supplementation. Arch Gen Psychiatry, 1974; 31: 547-552.
11. Hoffer A: Treating chronic schizophrenic patients. J Orthomol Med, 2002; 17: 25-41.
12. Kraft BD, Westman EC: Schizophrenia, gluten, and low-carbohydrate, ketogenic diets: a case report and review of the literature. Nutr Metab (Lond), 2009; 6: 10

Posted in Uncategorized | Tagged , , | Leave a comment

Unbelievable Wonders of Exercising the Brain–Proven effective in schizophrenia, depression, OCD, Autism (ASD).

Recently I read something new that I believe will be useful in the treatment of mentally ill. It has been tried on rats. Scientists produced schizophrenia like symptoms in rats by causing head injury in certain brain-area. The injury was given when rats were children. They grew normally. But they developed the symptoms later when they got to be what is equivalent to 20 years on human scale. Scientists then had the rats do some brain exercises and the symptoms were removed!!!  Imagine no psychiatric drugs, no special nutrition!!!

Another scientist has worked on human (not rats)  schizophrenic patients but the results using brain exercises are not yet established as definitely possible.  More work is going on.

I have a 2-part interview of John Nash. You know John Nash? The Hollywood movie “The Beautiful Mind” was on him. He was schizophrenic for over 10 years, relapsed two or more times, was repeatedly forcibly admitted in mental hospitals where he was forcibly given ECT (Electro Convulsive Treatment) and psychiatric drugs. But he never completed any treatment because all the times that he was hospitalized, he escaped from the hospital. He is no ordinary person. He is a Nobel Prize winner.

What does he say about what cured him? In the interview (I have the URL where his interviews are available) he gives sole credit to cognitive brain exercises on the computer. He also advises for other exercises such as chess and puzzles. His nobel prize is in economics and is famous for “Games Theory” taught all over the world in economics courses.

I have bought a brain exercise program. I and my wife have bought it to “fit” our brains. I recommend this program to everybody interested in brain fitness. Its based on the hard science of “Brain That Changes Itself” ( to quote the title of a book).

The same program has been tried by mothers on their autistic children. Autism is childhood version of adult schizophrenia but far more serious and worse than schizophrenia.  Mothers who report no effect have had their children do the exercise insufficiently. The mother who got really good result says she got the result with nearly one hour of practice (her autistic child practised the exercises), six days per week for nearly 2 months.

A former Ph.D.-student of mine who is Professor of Experimental Psychology in Institute of Psychiatry of the King’s College London has published a paper in the journal Brain. She has shown that with cognitive (exercise) therapy changes occur in the brain of schizophrenic patients as confirmed in fMRI (functional MRI).

Best wishes to all brains.

Ratan Singh (sometimes I sign as Ratan Sharma).,

Phones: 91-141-4022609,  91-141-2652561, 098281 99856,

Consultant in Nutritional and Neuro-behavioral Psychology, Jaipur Hospital, India.


Posted in Uncategorized | Leave a comment

Reverse the Brain Aging

Author’s Note: The article below, titled “Reverse Education”, has been published in the magazine Complete Wellbeing, Vol. VI, Issue 08, June 2012, on pages 74-75. Its a popular magazine available in metro’ cities and has its own web presence. I reproduce my article here with the editor’s kind permission. But, to relish this article in its original flavour, I suggest the reader should either pick up the June 2012 copy of Complete Wellbeing or get it in its digital format or read it on the web site of the magazine if and when the editor uploads my article on the magazine’s URL:  The photograph below is not mine (I am older)., 91 141 4022609


Reverse education

By Ratan Singh,

No matter how old you are, learning new skills can reverse
age-related deterioration of brain functions

In Australia, there is a college in which no one under
55 years of age is allowed admission. The idea is to
cater to the curiosity bug of the elderly. If an elderly
person wants to know how a pathologist takes red
blood cell count, a short course is arranged for him
that gives the senior hands-on experience doing it. Closer
home, a senior IAS officer sought government admission to
the first year of medical college. When his request was declined,
he enrolled for graduation in the science stream once
again. What we have here are people in their senior years
trying to learn. Are these perversions? Certainly not. They
are ways to maintain robust mental health.
Use it or lose it
Engaging your brain in challenging mental activities as
you grow older, slows down brain-ageing, keeps the brain
young and prevents Alzheimer’s disease and dementia. An
experiment with rats that had toys to play with showed that
they had more synaptic neuronal connections compared to
those rats that were deprived of such stimulation.
Brain exercises such as computer games, crossword
puzzles, chess, learning music or a foreign language and
memory exercises have been used to facilitate recovery frombrain damage caused by head injury, stroke, diabetes, infarct
and chronic schizophrenia. Back in 1915, American psychologist
Shepherd Ivory Franz showed that persons paralysed
for over 25 years were able to recover with brain-stimulating
Mental exercises can heal a sick brain. Scientist and
mathematician John Nash is a striking example. He was
seriously mentally ill, afflicted with schizophrenia for more
than a decade. He was hospitalised at least thrice because
he would escape each time and refused psychiatric drugs.
Nash famous for his “Game theory”, later on went on to win
the Nobel Prize in economics. In an interview, he specifically
attributed his recovery to brain exercises like chess and computer
games and calls this strategy ‘cognitive therapy’.
Do the new
Seniors who carry on working even after retirement often
boast of being ‘active’. However, this kind of being ‘active’
doesn’t help the brain because they are only exercising the
pre-existing old neuronal circuitry.
Old memories have had the advantage of repeated mental
practice or recall over the years. Therefore, the cliché,
‘old memories die hard’, holds true. They are the last to fade

away in dementia and Alzheimer’s. They are also stored in
locations distinct from recent memory. It’s during learning
that new neuronal connections are formed, says Professor
Merzenich from the University of California, San Francisco.
Learning a new language or trying a mid-age career
change involves having to learn afresh like a child, without
the advantage of prior experience at the task. Our brain has
to be in full focus on the task. This is hard work compared
to the brain work required for practising the old skill. More
neurochemicals acetylcholine and dopamine are released.
On such occasions, our brain is becoming younger, generating
new neurons!
Learn to change the brain
Once dead, brain cells cannot be brought back to life. However,
new brain cells can be formed. This is neuro-genesis.
And that happens when we learn a new skill.
When we are in the process of picking up a new skill,
new nerve cells are generated in the hippocampus. And depending
upon what brain region is engaged in learning the
new task, these young nerve cells migrate to the engaged
brain region and start to function in their new location.
It’s in the hippocampus that new mental associations, new
learning occurs before it’s shifted to higher brain regions for
permanent storage.
If you can’t practice a new skill physically, just imagine
yourself doing it. Scientists had one group of persons
practice a skill for a week and saw the improvement not
only in their performance, but also in the brain map of the
corresponding brain region. But this was expected. However,
what was unexpected was that the second group
that ‘practised’ the same skill in their minds, too showed
improvements in brain function and map. Admittedly, the

changes in the ‘mental only’ group were weaker than in the
first group but the point is that they had both structural
brain change and also improvement in their functional use
of the skill.
The brain is not a rigid structure but is easily malleable.
Changes in the level of mental stimulation alters neural
circuitry and consequently, the physical architecture of our
brain, keeping it young. So keep it engaged!
Tools to keep it sharp
Chess: Anatoly Sharansky, the famous Soviet human rights
activist of the late 1970s was imprisoned for his alleged spying
against the then-Soviet Union. He was imprisoned for
nine years, till eventually released due to political pressure
and sent to Israel, where he became a cabinet minister.
During his prison term, Sharansky kept his brain in
good shape by playing mental chess. He used to plan from
both perspectives—a rare mental effort. Without the mental
work, all his brain maps would degenerate. Several years
later, when world chess champion Gary Kasparov played
against the Israeli President and leaders of opposition in
Israel, he defeated all but Sharansky.
Crossword puzzles: A study of 469 people over 75 years of
age published in the New England Journal of Medicine, revealed
that 124 subjects who later developed dementia, over the
following five-year period, were the ones who were the least
active among the lot. The non-demented active seniors regularly
solved crossword puzzles, played board games, read
books and newspapers and participated in group discussions.
Music: Brain imaging of musicians’ brains shows that many
areas of their brains, such as the motor area [because they
use fingers] and cerebellum, are larger than those of the
non-musicians. Long-time musicians also have thicker fibres
connecting the left and right sides of the brain.

When approached with information on keeping the
brain active, most people say, “What do I have to
do with all this? I don’t have dementia or Alzheimer’s”.
Dementia doesn’t set in abruptly. It comes gradually.
Alzheimer’s takes ten or more years before it manifests
clinically. But soft signs start over a decade in advance…

When approached with information on keeping the
brain active, most people say, “What do I have to
do with all this? I don’t have dementia or Alzheimer’s”.
Dementia doesn’t set in abruptly. It comes gradually.
Alzheimer’s takes ten or more years before it manifests
clinically. But soft signs start over a decade in advance…

> You open the fridge but forget what for?
> You go to another room in your house but forget why
you came there?
> You forget the names of people you used to know?
> You frequently forget where you kept your keys, eye
glasses, pen or wallet?
> You need to use gadgets or a pocket diary to remind
yourself of important appointments or tasks?
> You get lost while talking…you stray away in circumstantial
details and forget the main argument with
which you started?

> You have to frequently ask your listener “So where was
I [or were we]”?
> You feel the name of an object or a person is ‘on the tip
of your tongue’ and yet, you can’t recall it exactly?
> In your hometown while driving you suddenly feel for a
moment that you are lost?

People with memory problems refuse to accept that
they have a problem and dismiss their failure to recall
recent events or learn new things as anything serious.
And sometimes even proudly declare that they can recall
even old events. The misconception here is ‘the older the
memory, the more difficult it is to recall’.
But this isn’t true. The capacity to learn new things and
recall recent events is lost more easily than the memory for
old events. It will be too late if we wait for the old memories
to switch off. So, start mental exercises as soon as you can.
For best results, provide optimal nutrition for the brain.

Ratan Singh is a certified behaviour therapist from late Prof. J. Wolpe’s Unit, Temple Univ
Med School, USA. His interests include Quantum Physics and its integration with spiritualism.
He was the religious advisor for Chinese Buddhist students of the University of Science Medical School in Pinang, Malaysia.

Stay Well
Have something to say? Send your comments and
suggestions to us at

VOL VI ISSUE 08  june 2012 p 74 and 75.

Posted in Uncategorized | Leave a comment

An Excerpt from my hospital notes on GFCF in ADHD

Author: Ratan Singh, DM&SP, Ph.D., phone: 91 141 4022609,  91 141 2652561, mobile: 098281 99856;,; Consultant in Nutritional & Neuro-behavioral Psychology, Jaipur Hospital, India.

Below is an excerpt, a leaf, from my hospital file notes on an ADHD child whom I had put on the home-based test for gluten and caseine. The test involves a short trial run of “GFCF”.
Pt. gave good response to GFCF diet test. The good effect of GFCF started on the 8th day of starting the diet.

Child’s mother noted the following behaviours and I also observed them in my office in the hospital: He was never at rest. He moved around, pulled things on my desk and rack. Screamed when stopped. At home didn’t allow touching his head while mother would oil his hair and in fact did not allow her to touch him at all. He would eat everything after smelling. Shuts ears when grinder is switched on.

He completed 15 days of GFCF diet on July 25. The testing started thereafter. The following is based on his mother’s verbal report that I noted in the case file in english language.

On eighth day of this diet he showed clear improvement. He obeyed simple commands. He never bit or scratched his sister. When he wanted to tell her to play with him but if she was sleeping under cover of bed sheet, he walked around and tried to pull the sheet. By contrast, earlier he would bite and scratch his sister. He stopped scratching his mother also. He started sleeping without any struggle or effort on the part of mother and sister. About 10 PM he would sleep without being cajoled and wake up about 5 AM. And for the first time ever in his life he started sleeping two hours in the afternoon on his own.

On July 26 and 27 his mother gave him lot of milk –as test dose– but the “no gluten” condition continued. Here are the results that the mother brought to me written in Hindi (that I translate into english):
“He stopped sleeping In the noon, started scratching and biting the mother (and sister if she was home). Sleep was disturbed. He did not sleep until 11 PM and that too under pressure and woke up at 2 AM and roamed from room to room and kept on asking for milk ( my comment: like an addict on drug withdrawal—here the drug was caso-morphine from caseine). Head banging two times”.

On July 28 and 29 milk was again stopped (gluten was already off). Results hand-written by mother, translated by me in english, are:

“July 28, a bit easy and bit peaceful. On July 29th slept at 1 AM, woke up at 4 AM. But viewed Tv peacefully”.

On July 30th (milk had been off from 28th) and 31st wheat was given as test. He was “normal” these entire two days. But stool (although only two times) was very very smelly and profuse.

Answer the questions below to extract maximum knowledge from the above case report.

Q1. Describe the ABA design if you think it was used at all in this brief report.
Q2. Aggression could be linked with milk or with wheat in this case report?
Q3. Was there any desirable effect of wheat withdrawal? Describe it if it was there.
Q4. What was MORE problematic: Wheat or milk?
Q4. What should be the future therapeutic plan?

Posted in Uncategorized | Leave a comment