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Saturday, December 28, 2013

Anaemia in Laywoman Terms - Last Post for 2013

2013 is coming to a close.  You would probably know that my writings mostly touch on matters that do not impact the immediate.  A complementation is therefore in order as I look forward to 2014.

Anaemia is age-biased - the highest incidence rate is in the little kids population segment.  It is gender-biased - women are at a much greater risk than men.  About 25% of the global population is anaemic.  Therefore there is a high chance that someone we know or care about is anaemic.  Non-life threatening direct effects of anaemia include fatigue, shortness of breath, headache, difficulty in concentration, mood swings and brittle nails.  In acute cases the impact can be a lot worse.  I think therefore a write-up on anaemia would be a perfect way to close 2013 and wish you and the world a healthier 2014.

I have tried to keep medical terminology to the minimal, used a 'matter-of-fact' language.  My idea was to explain anaemia in simple terms in the hope that it helps you enhance your two-way communication with your doctor if you or people you care about are anaemic.

The article is in three parts.  The first part explains metabolism - the cycle of life.  The second addresses the question about where anaemia (mis)fits in within the cycle of life.  The third covers risk factors that cause or increase susceptibility to anaemia.

1. Metabolism - the Cycle of Life
A living organism must breathe.  It must be able to regenerate cells to aid body growth and to replace worn out cells.  The first activity is called catabolism.  The second is anabolism.  Taken together the two are referred to with the far more familiar term - metabolism.

Metabolism is a cell-level activity.  Every living cell in the body participates.  It requires two external inputs:

(i) Food: Digestion starts at food ingestion and ends at absorption of nutrients into the blood stream.  Blood transports nutrients to cells where they are broken down into simpler substances.  The process of breaking down leads to two useful outcomes: A. Energy is released and made available for the body for uses as diverse as blinking to running away from a hungry bear.  B. Some of the simpler substances are critical building blocks needed for cell formation.  The breaking down of food particles that takes place inside the cells is colloquially called burning.

(ii) Oxygen: Burning is an oxidative process, i.e., it requires oxygen.  Carbons dioxide and other wastes are released during burning.  The blood carries the wastes from the cells to the lungs.  The lungs clean the blood and replenish its depleted oxygen content.  The re-oxygenated blood is transported back to the cells.  The metabolic cycle continues.  The cycle of life continues.

2. The Cycle of Life - Where Anaemia (mis)fits in
As we saw in the last section, for cycle of life to function at all, the digestive system must convert ingested food into simple nutrients that can be readily absorbed into the blood stream.  The respiratory system must oxygenate, detoxify and then re-oxygenate the blood.  The circulatory system must carry nutrients and oxygen to each cell in the body and carry waste out of cells and deliver it at the excretory organs.

Amongst these several functions, anaemia concerns the situation wherein body cells do not receive adequate supply of oxygen.  As we saw no oxygen means no burning; no burning means no metabolism; no metabolism means no life.

So far so good?  We are now ready to investigate what can cause problems in the oxygen delivery pathway.  Once we understand this we can enhance the second leg of the two-way conversation we ought to have with our doctors. 

3. Anaemia - the Risk Factors
We have heard of red blood cells (RBCs) and white blood cells.  If you remove these from blood you are effectively left with blood plasma - the fluid that gives blood its mobility.  Oxygen's solubility in plasma is rather poor.  Therefore it needs something to hitch a ride on to its way to the cells.  It needs a carrier.  This carrier goes by the familiar name haemoglobin.  Haemoglobin is a good carrier.  But oxygen is unable to directly latch on to haemoglobin.  It needs a latching agent.  The agent must have three properties:

(i) Oxygen must be able to latch on to it;

(ii) The agent itself must be able to bind to haemoglobin;

(iii) Once oxygen-laden haemoglobin is delivered to a cell then the latching agent must unbind and release the oxygen molecule to the cell.

This latching agent is iron.  Iron deficiency means inadequate supply of latching agents; which in turn means that enough oxygen cannot be transported to the cells; which in turn means inadequate metabolism; which in turn means insufficient energy generation and inadequate replacement of worn out cells.  In short, this means anaemia.  Eureka!

Thus, the 1st risk factor is iron deficiency.  Let us move on to the second.

Assume one takes adequate quantity of iron in food.  However one's diet patterns may include co-consumption of generous servings of calcium-rich foods such as yoghurt or cheese.  Furthermore many of us like soft drinks with meals or wrapping up the meal with a cup of strong coffee.  These foods inhibit the uptake of iron by the body.  It is not the amount of ingested iron that is important but how much actually gets absorbed, especially if one's iron uptake system is under-performing.  If one already has iron deficiency then one may want to space the consumption of the other foods so that iron does not have to compete with those for being absorbed.  For example coffee is absorbed within about an hour.  But depending upon your source of iron, iron absorption could take several hours.  Thus one may drink coffee up to an hour before having iron-rich food or wait for 3-5 hours after a meal before refilling one's cup or reaching out to a soda can.

Co-consumption of calcium or caffeine rich foods is the 2nd risk factor.

The most commonly occurring haemoglobin complex in our bodies holds four iron atoms, i.e., has four latching sites.  Thus four oxygen units can latch on to a single haemoglobin molecule.  Haemoglobin however does not float freely in blood.  Haemoglobin is contained in red blood cells (RBCs) - everything is packaged!  Thus if the RBC count in blood is low then the amount of haemoglobin in blood will also be low.  In that case we would have fewer latching agents (iron atoms) and thus fewer oxygen molecules can be carried per unit volume of blood.

Thus low RBC count is 3rd risk factor.

Let us say one's intake of iron is adequate, one's absorption of iron is adequate and one has a normal RBC count.  Essentially, one has jumped through the first three hoops.  What then?

Well, oxygen must bind to haemoglobin at the iron site.  However the iron site within haemoglobin does not have an affinity for oxygen alone.  It can also bind to carbon monoxide, nitrous oxide or hydrogen sulphide.  In fact iron sites have 250 times the affinity for carbon monoxide than it has for oxygen.  Once haemoglobin binds to one of the other gases it is unavailable for carrying oxygen.  One may be exposed to these gases due to pollution or smoking.

Thus the 4th and 5th risk factors are pollution and smoking.

Let us say one manages to jump through the fifth hoop as well, and land on one's feet!  In that event an adequate number of oxygen molecules have hitch-hiked and are on the move.  Just as traffic slows us down leading to an upset partner or impatient kids, RBCs can be slowed down as well, especially at bends in narrow capillaries.  Promises to pick up groceries or ice-cream topped with crunchy nuts on the way do not work :-).  If oxygen cannot be delivered at an adequate rate then metabolism will slowdown.  To avoid slowing down in the bends and narrow alleys the RBCs must be elastic.  Haemoglobin forms 95% of an RBC's dry content.  Thus for an RBC to be elastic the haemoglobin must be elastic.

A genetic disorder called sickle cell disease causes haemoglobin to lose elasticity and distort from its usual round shape to a crescent shape.  This causes two problems - the 'last cells' are perpetually starved for oxygen and the wear and tear of RBCs increases.  In worst cases of sickle cell disease, mean life of an RBC falls to just 10% of a normal RBC.

Thus sickle cell disease is the 6th risk factor. 

RBCs may also lose their elasticity if the body is frequently exposed to altitudes greater than 3000 meters without adequate acclimatization.  Thus inducing an affliction similar to sickle cell disease.

Thus frequent exposure to high altitudes without adequate acclimatization is the 7th risk factor.   

Thalassemia, a genetic disorder, can cause severe anaemia.  It induces RBCs to shrink in size.  As a result haemoglobin production is reduced.  The cell pressure increases causing RBCs to rupture.  Chronic iron deficiency, especially during childhood years can also cause RBCs to shrink and lead to their easy rupture.  If that happens blood's capacity to carry oxygen is reduced.

Thus Thalassemia and chronic iron deficiency during childhood are 8th and 9th risk factors. 

Most of us would easily beat the seventh hoop though it takes some work and also gene-luck to beat the other eight.  Let us say one is able to do that.  So now oxygen in adequate quantities is reaching the last cells.  Can we now uncork the champagne?  No.  Not yet!  Remember the oxygen was carried to its destination precisely because it remained latched on to iron which in turn remained bound to haemoglobin.  The time has come now for the haemoglobin complex to unbind and release the oxygen to the cell.  High blood sugar levels inhibit this release.  Blood sugar levels may remain elevated for a considerable time if excessive amounts of sugar is consumed.  Diabetic patients tend to have chronic, high levels of sugar in the blood.  Alternatively excessive alcohol consumption substantially lowers effectiveness of insulin to regulate sugar levels leading to elevated sugar levels.  With high sugar levels oxygen will merely make a round trip - lungs to blood stream - and then back to lungs without being released in the cells.

Thus we have our 10th, 11th and 12th risk factors - excessive consumption of sweets, diabetes and excessive consumption of alcohol.

A dozen is a good place to stop - one for each month of the year.  Have a fulfilling 2014.

Amit

Saturday, July 27, 2013

Moose Safari in Sweden

For once, I turned into a wildlife traveller in Europe.  I visited Sweden to see moose - the largest deer on planet Earth.  Here is my trip report.  But first, a short note on tapering of quantitative easing (QE) in the US.

The US Feds have dropped hints that they might decrease the quantum of QE.

The QE Santa Claus has visited many homes - commodity markets, bank balance sheets, mortgage markets, auto industry and the treasury in the US, the European Central Bank (via euro-dollar swap lines), emerging market corporate and sovereign bond markets, global equity markets, groups that spearhead human rights around the world - the list is long.

The ECB remains in need of the swap lines.  The US mortgage markets remain afloat mainly due to continuing QE.  Increasingly, the US fiscal and trade deficits are  being financed by the QE as China is seeking more and more real assets as a payback for its exports and petroleum-rich Arab countries continue to diversify away from US-based assets following the twin geopolitical shocks of 9/11 and the Arab Spring.

The QE quantum stands at $85bn a month.  I think in the immediate term (about 1y) a tapering of the order of $15-25bn a month is possible, mainly as the rise of shale gas has induced a fall in trade deficit and the US banking sector has regained a fair bit of stability.  For a materially larger taper I would watch out for the following; without one or more of these significantly greater and sustained tapering is not possible.
 
- material increase in taxes,
- sharp fall in trade deficit,
- sustained weakness in the Dollar vs other currencies,
- high consumer price inflation
- willingness on part of the ruling elites to accept material deflation in asset prices
- tapering of currency swap lines with the ECB
 
Yours, Traveling Ec0n0mist,
 
Amit
 
One night?  Sure.  You can slip into a sleeping bag in a 7 x 9 ft wooden lodge or spend the night in (again) a sleeping bag in a 6 x 7 ft observation tent.  That will be £160.  How would you like to pay?
 
I bet this would make people drop the idea, hang up the phone or reach out for their delete button.  Well don't.  Here is why.
 
Jan and Marcus run Wild Sweden tours.  Jan brings with him intimate knowledge of local wildlife, their habitat, their movement patterns and what an enthusiast must avoid in order increase her chances of spotting the animals.
 
A moose can hear you zip (or unzip) from a kilometer.  Those with large antlers have even better hearing.  It can smell you from about the same distance.  You can spot a moose in darkness by shining floodlights into its eyes as they reflect rather bright.  Shining light into their eyes does not startle them.  Those who like alcohol while they wait for the moose to turn up, Jan will include some.  Having told  the Do's and Don'ts, he will leave you in an observation tent with a sleeping bag, a chair, a pair of binoculars, boots and a basket of food and drinks.  To my delight he made sure the food included local flavors.  After about 3 hours of waiting I saw a moose calf and then, a moose bull. To see them in the wild is thrilling. You also feel an immense sense of achievement in that your presence went unnoticed by the moose's sharp senses.  Once a moose is there it could easily spend 2-3 hours grazing in the same area.  This will give you enough time to photograph and observe Moose behavior.  I clicked a few hundred photographs of which about 10 turned out to be decent.  This speaks more about my fledging skills at wildlife photography than about the real difficulty in photographing moose.  Time permitting I will make another post about tips on Moose photography.  I wish I could pick those up before I got into the tent!  
 
After it got too dark to photograph, Jan drove back to the tent to pick me up for a drive by the forest and nearby fields to see even more Moose.  Armed with a floodlight we spotted eight more of them.  I was rather pleased with his patience as late at night as I frequently struggled to mount my camera on my new tripod in the darkness.  Finally we drove back to Kolarbyn Ecolodge.
 
Andreas runs Kolarbyn Ecolodge.  In the right season the place is abound with blueberries, wild mushrooms and croaking frogs.  He has fashioned it to be so eco-friendly that apart from a layer of plastic sheets to keep the rainwater away from dripping into the lodge, there is little else about the lodge that would leave a mark on the environment. He prepares the charcoal needed for fire, uses untreated wood to build the lodge in order to prevent chemical leakage and sources eco-friendly food from local suppliers.  Building lodges with untreated wood means that he has to build them afresh every 2-3 years.  Buying from local suppliers is rather expensive as the decade long move towards integrating European agro-markets has driven Swedish farmers out of business.  Those who remained in business became substantially more expensive as farm support systems have weakened considerably and consumer profile has changed from an average Swede to those who choose local produce to ensure what they eat meets the highest standards of eco-friendliness.

I joined Jan for a Moose tour though he does regular wolf, bear and beaver tours as well.  He mentioned it is often difficult to spot a wolf though his visitors often get a chance to hear wolf howls as they howl back at his imitation of the howling sound!
 
The place is 2.5 hours from Stockholm Central station by train + a bus ride.  In order to arrive at the starting point take a train to K√∂ping (pronounced as 'sherping') and then a connection bus to Skinnskatteberg (pronounced as 'hvin-skatt-bare'). If you tell him your arrival time in advance, he will likely be able to arrange a pick-up.
 
For the service you get, the rather unique eco-friendly living experience, local food and the (near) guarantee of spotting Moose, the largest deer on planet Earth - I think you should pay Andreas and Jan a visit the next time you are in Sweden. 
 
All pictures were taken with a Nikon D7100 and a Nikkor 18-300 lens  mounted on Velbon ultrek ut-53d with QHD-53d head.  The moose was about 100 meters from the observation tent.
 
A mouthful: Just like a cow, a moose's stomach has four parts.  It can eat about 30 kg of vegetation a day.

Grazing posture: A moose spreads or bends its forelegs while grazing .  This moose is rising back to its normal posture just after taking a mouthful.  

Moving one ear: A Moose can move its ears independently.  I had set the camera to slow shutter speed as natural light was dim.  Therefore I fortuitously captured the motion blur of its right ear flapping.  

Looking straight at the observation tent: Its not the look that will get you but your odor or the sound you make.  A moose's eyesight is not only poor but it has a huge blind spot right in its front view.

Night shot: This looks like a relatively young moose as its coat is still light in color.  

Moose Shine: A moose's eyes reflect light particularly strongly in the yellow wavelength.  Human eyes reflect the red wavelength.  Therefore cameras are equipped with red eye reduction feature. 

Moon light: The moon barely rose above 40 degrees.  Conifers look stunning with a full moon in the background. 

Kolarbyn Ecolodge: I am told that the ecolodge concept draws heavily on how miners and loggers lived for centuries when they would camp out in the woods. 

Blueberries: They are all over the lodge.  They are ready to be plucked in August.