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It begins with RNA Which calories are the worst? Clostridium difficile Artificial Sweeteners
It begins with RNA
picture has been that DNA runs the show as far as cells and organisms
are concerned; that is where the blueprints and the command center
are located. RNA has been considered the little brother who acts as a
go-for, carrying messages and fetching things. The two types of
nucleic acids do not differ a great deal but seem very distinct in
So... DNA can
store information in a very stable way but not much else, RNA can
store that same information and also can act like a protein
catalyze some important reactions. This multi-role of RNA is seen
in the making of protein according to a DNA 'gene'. First a molecular
machine (mostly protein but with an RNA core) runs along the DNA and
creates a RNA copy. That messenger copy called m-RNA is then modified
by another protein-RNA machine called a spliceosome. The modified
m-RNA travels out of the nucleus of the cell and is taken up be
another molecular machine, the ribosome (mostly protein again but
with an RNA core called r-RNA). The messenger strand is feed through
the ribosome, indexing one 3 letter code at a time. Another type of
RNA called transfer RNA or t-RNA holds amino acids at one end and the
3 letter matching code at another end. There is one type of t-RNA for
each amino acid. In the ribosome the t-RNA sticks by its code to the
code of the m-RNA that is in the active area and while it is held
there, the r-RNA joins the amino acid that the t-RNA is carrying to
the previous amino acid to lengthen the protein by one amino acid
unit. The m-RNA is then indexed by one code and releases the empty
t-RNA while exposing the next code for the appropriate t-RNA. After
the m-RNA has made the number of copies of the protein required,
other RNA marks it and it is destroyed.
- DNA forms a double helix and is not normally a single
strand. RNA is single stranded, although it often curls back on itself
and forms short bits of intrastrand double helix. These gives RNA
molecules somewhat rigid shapes.
- The sugar backbone is deoxyribose in DNA and ribose in
RNA. This makes RNA less stable than DNA and it can be destroyed by
- The four bases (adenine, thymine, cytosine, guanine) are
the 'letters' (ATCG) of the DNA code with 3 letters standing for a
particular amino acid in the protein molecular being coded. In RNA the
thymine base is replaced by uracil.
- The bases of RNA are often modified after the RNA is made
so that it can be used for special tasks. There are over a 100 small
changes that can be made to the to an RNA molecule.
- Because it can have rigid shapes, RNA can act similarly to
a protein enzyme and catalyse reactions. The most important is the
'enzymatic' action of RNA is to form peptide bonds and therefore create
Since the genome
was read a few years ago, it has become apparent that there are a lot
more RNA encoded in the DNA then the RNA involved in making proteins.
RNA is very active in controlling the use made of DNA genes. The
number of letters like m, r, t in front of RNA has blossomed. Instead
of RNA being the little brother go-for, it is more like the
librarian. It has this large DNA library which it polices and
publishes as required. It controls the production of the thousands of
proteins, which are considered the work horses and structural
building material of the cell. The list of types and roles of RNA has
become very long.
noticed that ribosomes could be the foundation of life. If something
can code for itself and for the enzymes needed to make itself then it
can be a self-replicating machine and can slowly evolve a complex
cell to live in. RNA in the form of a primitive ribosome can be the
start of life. Their questions were how much is the ribosome
conserved across the whole of life or in other words how old is it
and is the RNA needed to make a ribosome held within the ribosome
(even if it is no longer used). They looked in the r-RNA for t-RNAs
and the m-RNAs needed for the ribosomes own proteins.
organic chemists anthropomorphize molecules, they say that molecules
"want to be in their lowest energy conformation." This
means that when they have energy molecules can move into different
conformations, but they have a resting position that they come back
The resting position of DNA is very
tightly curled up. It is so hard to unravel that researchers do not
fully understand how the various helper molecules uncurl and unzip it
for replication and translation.
From the organic chemistry point of
view, the answer to "what does DNA want" is: It wants to
sit curled up in a knot. DNA does not want to replicate or translate.
The conclusion that DNA was unlikely
to be the dynamic mover of evolutionary processes led to the next
question: So who does want to do replication and translation?
To Meredith and Robert
Root-Bernstein the answer is clear: the ribosome. Its resting
position is "ready to translate DNA into proteins." And not
only are ribosomes found in all cells of all organisms, they are
almost identical in all living species.
What if ribosomes are "selfishly"
trying to reproduce themselves? Did ribosomes recycle ribosomal RNA
to interact with proteins--creating the mRNAs and tRNAs we know
today-- and invent DNA as securely stored assembly instructions? If
this were the case, then the rRNA sequences should match the
sequences of mRNAs, tRNAs, and DNA encoding ribosomal proteins.
This new hypothesis was tested by
Robert, comparing ribosomal RNA to databases of all the RNAs, DNA and
proteins of the bacteria E. coli.
If ribosomes want to reproduce
themselves, the rRNA would have to contain three things that no one
has ever noticed before. First, it must contain the "genes"
encoding its own ribosomal proteins so as to be able to form a
working "machine." Second, it must contain the mRNAs needed
to carry its own genetic information to the "machine."
Finally, it had to encode the tRNAs necessary to translate the mRNAs
Meredith and Robert Root-Bernstein
showed that the structure of the rRNA shows startlingly good matches
to all of these structures in E. coli.
"We have demonstrated that rRNA
contains the vestiges of the mRNAs, tRNAs and "genes" that
encode its own protein structure and function. Ribosomes are not
simply the passive translators DNA," says Dr. Robert
The selfish ribosome model closes a
big theoretical gap between, on the one hand, the simple biological
molecules that can form on mud flats, oceanic thermal vents or via
lightning, and on the other hand LUCA, or the Last Universal Common
Ancestor, a single-celled living organism.
Dr. Meredith Root-Bernstein adds:
"Maybe the selfish ribosome puts a new spin on feeling kinship
with other creatures. We are all just different kinds of homes to the
Which calories are the worst?
There has been a disagreement over
whether fats or carbohydrates are the better or worse way to get
calories. Of course everyone agrees that we need some fat and some
carbohydrates and that there are better and worse sources; and
everyone agrees that you can take in too many calories – also too
few. But there the agreement seems to end and individual scientists,
physicians and nutritionists can have very different views.
The fat-is-not-the-problem people keep
popping up although it has been a dangerous thing to say and
sometimes people lose their reputation. The food industry had a lot
invested in 'low fat' and also in 'sugar added', as well as artifical
sweeteners. They and agriculture resisted any attack on
carbohydrates. But there is always someone who has their proof that
the problem is not fat or that the problem is carbohydrate. The
official advice has been anti-fat and often pro-carbohydrate
throughout almost 50 years.
Some information has come to light that
helps to explain the durability of the pro-carbohydrate camp. Now it
turns out that many of those giving advice were 'bought'. “Public
health scientists and a government committee working on nutritional
advice receive funding from the very companies whose products are
widely held to be responsible for the obesity crisis, an
investigation by The British Medical Journal reveals. Recipients of
research funding from sugar and other related industries include
members of the Scientific Advisory Committee on Nutrition, which is
currently updating official advice on carbohydrates consumption, and
researchers working for the Medical Research Council's Human
Nutrition Research unit. Findings from the special report raise
important questions about the potential for bias and conflict of
interest among public health experts as the UK faces a growing
obesity epidemic.” These scientists “have received research
funding and funding in kinds from companies including Coca-Cola,
Mars, Nestlé, Sainsbury's, the Institute of Brewing and Distilling,
Weight Watchers International and others. As a former HNR researcher,
Susan Jebb, professor of diet and population health at the University
of Oxford and chair of the government's Responsibility Deal Food
Network, received support for her work from Coca-Cola, Sainsbury's,
Cereal Partners and Rank Hovis McDougal, among others. Between 2008
and 2010, Coca-Cola donated £194,000 to one research study on which
she was the principal investigator. Listed as sole or co-principal
investigator on 10 industry supported research projects between 2004
and 2015, Jebb attracted funding worth £1.37 million to the HNR
unit. Some of the companies that supported her work at HNR, including
Unilever and Coca-Cola, are now members of the Responsibility Deal,
which Jebb chairs. .... Similarly, research carried out by members of
the Scientific Advisory Committee on Nutrition has been supported by
companies including PepsiCo, Coca-Cola, Mars and Nestlé. An analysis
of the annual declarations of interest by SACN members shows that
between 2001 and 2012 there was an average of 45 declarations each
year involving companies from the food, drinks and pharmaceutical
industries. Of the 40 scientists affiliated with SACN between 2001
and 2012, only 13 have had no interests to declare. David Stuckler,
professor of political economy and sociology at Oxford University,
says the engagement of companies such as Coca-Cola with the work of
public health organizations "falls into the category of efforts
to crowd out public regulation, to try to weaken public health by
working with it."
The Responsibility Deal is not working.
Industry's pledges do not add up to the government target of 5%
reduction in calorie consumption and the calories in the national
consumption rose between 2006 and 2014 by 12%.
Information from J. Gornall. Sugar:
spinning a web of influence.
BMJ, 2015; 350
Clostridium difficile tends to strike following antibiotic
treatments. And the other known 'fact' is that people got it in
hospital but that hospital's could not seem to get rid of it no
matter how they cleaned. People die of C. difficile directly or
because it damaged organs (heart, lungs, kidneys) in already weakened
patients. It happened to my brother George. The doctor implied that
(1) George was in very bad shape with diabetes, kidney failure and a
damaged shoulder from a fall (2) he suffered from Cdiff during
recovery but he didn't come in contact with it when in hospital (3) he was put in
isolation and when his Cdiff was almost cured and he was going to be
out of isolation in a short while (4) his heart failed and that
killed him but really he died because of the Cdiff and other sources
of damage to his heart. Recent scientific news helps make sense of
Many people have Cdiff in their gut and it causes them no harm. It
is only went the organisms produce their toxins that they cause
disease. So people who coming into hospitals (patients, visitors,
staff) often carrying Cdiff. The doctor was probably right that
George brought his Cdiff with him. I think George was given
antibiotics for his kidney problem and that would have triggered the
Antibiotics encourage Cdiff to produce toxins. How? Many types of
bacteria are able to do something call 'quorum sensing'. They can
communicate and in doing so, they can judge would plentiful they are.
This judgment then affects their choice of behavior. Bacteria can
also sense how much nutrient is around them. If Cdiff cells sense
that there are a lot of them (unusually high numbers) and they are
running out of nutrients, they produce toxin.
So how do antibiotics produce lots of Cdiff running out of food?
In normal situations, this does not happen in the gut. There is not a lot of Cdiff and there is food. But
antibiotics kill many types of organisms in the gut, as well as the
particular type they are aimed at. However, they are not very good at
attacking Cdiff and so the Cdiff are left with little competition for
food. Cdiff has a population explosion and then faces the problem of
eating themselves out of house and home. That is when they start
producing toxin. That toxin (toxins actually) cause illness and often
death. The patient is probably compromised to begin with and so is
less likely to recover from the Cdiff attack.
It has been shown a number of times in animals that eating
artificial sweeteners compared to sugar leads to increased weight
gain. This seems very contradictory and has been largely not taken
seriously by the public. Now there is another study with these
results but also with an explanation of how this could be.
In the new experiment, “10-week-old mice were fed a daily dose
of aspartame, sucralose or saccharin. Another cluster of mice were
given water laced with one of two natural sugars, glucose or sucrose.
After 11 weeks, the mice receiving sugar were doing fine, whereas the
mice fed artificial sweeteners had abnormally high blood sugar
(glucose) levels, an indication that their tissues were having
difficulty absorbing glucose from the blood. Left unchecked, this
“glucose intolerance” can lead to a host of health problems,
including diabetes and a heightened risk of liver and heart disease.
But it is reversible: after the mice were treated with broad-spectrum
antibiotics to kill all their gut bacteria, the microbial population
eventually returned to its original makeup and balance, as did their
blood glucose. ”
So it looks like it is the bacteria in the gut that are creating
the paradoxical result of artificial sweeteners causing obesity. The
bacteria that flourished in the artificial sweetener fed mice are the
same as those that flourish in other mice with forced or genetic
obesity. Gut bacteria mostly belong to two groups: Bacteroidates and
Firmicutes. In obese animals the Bs are less than normal and the Fs
more by around 50%. Changing the ratio by transplanting one of the
other type, changes the weight. It seems the Fs extract more
nutrition from food, manipulate epi-genetics to favour storing fat,
and possibly have an effect on some appetite hormones.
Does this apply to humans? Researchers tested “the association
directly in a small group of lean and healthy human volunteers who
normally eschewed artificial sweeteners. After consuming the U.S.
Food and Drug Administration's maximum dose of saccharin over a
period of five days, four of the seven subjects showed a reduced
glucose response in addition to an abrupt change in their gut
microbes. The three volunteers whose glucose tolerance did not dip
showed no change in their gut microbes. ”
So if you are trying to lose weight, avoid artificial sweeteners
and just use less, maybe much less, sugar.
This was written for a different purpose but I am putting in this
Pain is complicated! I have attached a diagram that illustrates a
lot of the elements in the causes and reliefs of pain. Below is a
very simplified description of how it works.
- There are pressure and heat sensing nerve endings all over
the body but they do not signal pain. Special heat and chemical
sensors do that and they only respond to extreme (dangerous) levels
of heat and chemicals. The chemicals that trigger them are those
that are released by actual tissue damage, by inflammation, and by
strong acids. And there are two types of communication used by the
pain receptors – a quick short signal type that gives prick-like
signals and slow long-lasting ones that give burning or throbbing
aches. I think this is just the tip of the iceberg as pain receptors
are isolated small cells (not like eyes or ears) and probably there
are other types and divisions that have not be identified. There is
talk of a special kind on the palms of the hands that act up in ME.
- The receptor cells have axon extensions that go to the spinal
column and deliver their signal to spinal neurons. Then there are
relay stations along the way once the signal reaches the brain –
in the hind brain, the mid-brain, the thalamus and finally the
signal is sent to the cortex. At any one or all of these transfers,
the signal can be modified (strengthened, weakened or sent to a
different part of the cortex. There are various chemicals that can
affect the pain signal, particularly morphine and its naturally
produced twins, the endorphins. Again, this is probably far from the
whole picture. I believe people are discovering other paths to the
brain and other effects on the signal on its way to the brain.
- It only becomes a 'pain' in the real sense when it is
consciously perceived. People do not feel pain when they are asleep
and will feel less pain when they are preoccupied with something. If
the pain is the focus of attention then it will be stronger. Drugs
(also meditation and some activities) can be effective at this point
in lowering anxiety and stress, diverting attention and therefore
lowering pain sensations. This is a different intervention than
'pain-killers' that interfere with the nerves delivering the pain
signal. Placebos, acupuncture and 'magic' probably work at this
level but they also can increase endorphins by some unknown
mechanism that may include affecting the signal transmission to the
brain. Fatigue can lower the ability to control the emotional
reaction to pain and negative emotional reaction to pain brings it
into the focus of attention.
- Levels of pain do not stay constant. Pain can become stronger
even though the damage has not changed, and also can become weaker.
Some pain appears to have no real cause. Some pain remains even when
the source is gone. One way this happens is well documented.
Constant pain for a period of time causes a reaction in the sense of
touch. The ordinary touch sensors become very sensitive. If you
think about a red inflamed area on the body – you cannot touch it
without feeling a sharp pain. This touch would normally be way, way
to soft too cause pain receptors to fire. It would normally not be
painful to the touch sensors because it is barely a touch and anyway
they do not report pain. But the two receptor systems seem to
cooperate to register a sharp pain; they have become very sensitive.
Changes in the level of input to the brain has effects too. For
example, sensory deprivation causes hallucinations, like - “I'm
getting no signals from the eyes – I'll make some up”. Tinnitus
is thought to be caused by not being able to hear certain
frequencies all of a sudden. “I'm getting weird signals from my
ears, I'll stick in some of the missing sound”. In amputation,
the lost limb seems to have pains. “I'm not getting an sensation
from my leg, something is wrong, I'll assume it is painful.”
- Tissue repair can give pain. It is usually an itch but can be
a pain. There is a lot of swelling and shrinking, pulling and
pushing in some healing. A person can feel these sensations or can
also feel itchy and even pain. There are effects from changes in the
use of the injured area. Non-use can cause buildup of waste etc. in
the tissue and that can irritate the pain sensors. Healing tissue
may also use pain as a protective mechanism – in this case what is
needed is confidence that there is healing and everything is under
control and improving. In other words the body needs to believe that
protection is no longer needed. During healing it can be important
to get the level of activity right – not too little and not too
much. It is hard to guess the right level. It should not be – feel
good so work hard so feel rotten so stop all activity so feel
good... What is wanted is a half step forward and no step back,
rather than 1 step forward and 1 step back, or 2 steps forward and 3