Outten The Fire Within

   This blogs  shouldn’t take away  anything  from  the blog post  within      blog roll.  In  September,  I’ll attempt to bring  forth the information that        I  consider  redeemable  providing  cause n’ effects  and  how  it  prevents cancer  in  the  first place.  However, it’s  also  important  to  realize  that   you  will have to do your own research….  to fully understand the jest 0f  each blog post  which should take you a half  hour to read, checkout and  bookmark the links you  find interesting.

    What  does  a  stubbed toe  or  splinter  in  a  finger  have  to  do  with  Alzheimer or succumbing to cancer. As scientist scurry and delve deeper, they’re  starting  to  see a link to an age old  “defense mechanism”  called, chronic inflammation  ~  the same process that turns the tissue around a splinter ‘RED’ and causes swelling in an injured toe.  So with this really being the case can inflammation cause cancer?

     While causing a injury to  fend – off  bacteria, viruses, parasites and infections.  The moment a potentially deadly microbe slips into the body, inflammation  marshalls,  an attack  that lays waste to both invader and   any damage tissue it may have infected.  Every once in a while, however, this  feverish production  doesn’t  shut down  and  inflammation becomes chronic.

    When this happens the body turns on itself  and  in  recent years  this chronic  inflammation  has  become  a  ‘HOT’  topic  amongst  researchers. Research  shows  that  chronic  inflammation  does  harm  in  many  ways;      it can destabilize cholesterol deposits in the coronary arteries, potentially leading  to  strokes  or  heart attacks.  Also  it  chews up –  nerve cells in the brain  of  Alzheimer patients  and  fosters  proliferation  of  abnormal cells turning them cancerous.

    To  better  understand,   it helps to know  a  little  about  what  happens when the body is subjected  to  trauma  or  injury.  As soon  as that splinter slices  it’s  path  into  your  finger,  sentinel cells  stationed  throughout  the body alerts the immune system;  of the presence of  bacteria that may have come along  for the ride.  Some  of  those  cells,  called  mast cells,  release a  chemical called  “histamine”   make nearby capillaries leaky.

    This allows small amounts of  plasma  to  pour out,  slowing  down  the   invading bacteria  and  prepares other  faraway immune defenders to rush  to the scene of  the injury.  Mean  while  another  group  of  sentinels,  called macrophages,  begin a counter attack  and  releases cytokines which signal for  reinforcements.   Soon,  wave –  after – wave  of  immune cells  flood  the site,  destroying pathogens  and  damage tissue alike.

    NOT  long ago,  doctors thought heart attacks were results of  a molecule called LDL,  the  so called, ‘bad cholesterol’  providing the raw material  for fatty deposits; that slowly build up inside major coronary arteries causing blockage. So clearly, anyone with high LDL cholesterol levels where prone and  at a greater risk  for developing heart disease.  Although,  nearly half  of  all heart attacks occur in people with normal levels.

    In  the  early  1990’s,   Dr.  Paul  Ridker,  a  Cardiologist  Specialist  at Brigham  and  Women’s  Hospital,  in  Boston,  Massachusetts  discovered  an  inflammatory  reaction  was  responsible  for these  bursting  plaques.    To  test  his  theory,  Dr.  Ridker  needed  a blood test  that could serve as a  marker  for chronic inflammationHe settled on C- Reactive Protein CRP,     a molecule produced by the liver in response to inflammation.

    Inflammation harms the heart  when  levels of  CRP  reach  3mg/L  or  higher;  these amounts triple the rate of  heart disease.  By contrast  folks with extremely low levels of  CRP,   less  than  o.5mg/L  rarely  have heart attacks. Dr. Ridker  also says, “cholesterol deposits, high blood pressure, smoking will all contribute to the development of  under lying plaques.”

    What inflammation seems to contribute is in the propensity of  those    plaques to rupture and cause heart attacks.  At the very least,  high CRP levels  might  tip  the  balance  in  favor  of  aspirins  and  statins  known  to lower inflammation.  As well as  metaformim  that works to dampen inflammatory response in diabetics.

   Thereby, what researchers  found to hold true about diabetics are a complex  inter-play  amongst inflammation, insulin  and  fat. Either in       the  diet  or – in  large  folds  under the skin ( fat cells  behave  a lot like  immune cells  ~  spewing  out  inflammatory cytokines  particularly as       you gain weight when you age.)

     Dr. Steven Shoelsona researcher at the Joslin Diabetic Center in    Boston has bred a strain of  mice whose  fat cells are super charged  in inflammation  factories. These mice than became less efficient at using  insulin  and  go onto develop diabetes (thereby, inciting inflammation  producing diabetes.)   Also,  back in the 1860’s,  renowned pathologist  Rudolph Virchow,  speculated  that cancerous tumors a rise at the site           of  chronic inflammation.

     Now a days researchers are exploring the possibilities mutations            and inflammation,  are  a  mutually  reinforcing  process  that  is  left  unchecked  can  transform  normal cells  into  tumor cells.  Therefore,       how might this happen?   Some of the most potent weapons produced            by  macrophages  and  inflammatory cells are the so  –  called  oxygen         free radicals.  These molecules devastate any thing that crosses their        path….  particularly DNA.

    It’s a glancing blow:  damaging…. but  doesn’t  destroy a cell that       could lead to a ‘genetic mutation’  that allows it to keep growing and dividing.  To  the  immune system,  this  abnormal growth looks very      much like a wound that needs to be fixed and when the immune cells           get called in,  they bring with it growth  factor,  that says heal, heal,         heal.  However, with damage DNA involved it might cause it to grow          and divide abnormally while transforming into cancer.

    Another interesting aspect of  chronic inflammation  is that other researchers have discovered,  glial cells  can  produce inflammatory cytokines;  that call additional immune cells into action.  These glial          cells, sole purpose is to nourish  and  communicate with the neurons              of  the brain.  Thereby,  when you get a chronic activation which is a  process seemingly out of control…. it  than  does  result  in  a chronic inflammatory state.

     Therefore,  the best approach  to  reducing chronic inflammation               and  dampen  the  damage that’s done.  Is through losing weight with    regular exercise  ( 30 minutes  a  day  most days  of  the  week.)  While      fruits,  vegetables and  fish are great choices in a proper ratio of  fats, protein and carbohydrates that disable  ‘free radicals’ through intake            of antioxidants in a macrobiotic diet  (that lowers inflammation  and  maintains  a proper pH Balance  in your body.)

     Also  in  1996,   the  Journal  of  the  American Medical Association published the results 0f   a multi – centered,  double blind, randomized placebo controlled cancer trial base  on  20ug/day selenium or placebo          to 1,312  patients over a mean period of  4.5 years.  The  study  reported          a  50%  decrease in total cancer incidence,  as well as,  a  63% reduction         in  prostate  cancer,  58%  reduction  in  colorectal  cancer  and   a  48%  reduction in lung cancer.

     Selenium  has  so  many  anti — cancer actions  that it is difficult to establish  which  ones  are  predominant.  Selenium  also  helps  reinforce  glutathione levels  (considered the Master Antioxidant),  oxidative stress, DNA methylation,   DNA repair,  also  inflammation,   apoptosis,  and  cell  proliferation, carcinogen metabolism, hormone production, angiogenesis   and  immune  function.  Selenium deficiencies  (like  folic acid)  can  result   in decreased DNA methylation, therefore, increased DNA damage and mutation.

    Selenium  also promotes  the activity  0f  P53 protein,  which is 0ften    called, “the guardian 0f  the genome.”  Well over half 0f  all cancers have defective P53 protein. When  DNA is damaged, P53 either stimulates DNA repair  or  causes cells to self  destruct  (apoptosis)  if  the DNA damage is irreparable.  The  thioredoxin  reductase  system  promote  P53 induction      0f  DNA repair enzymes, therefore, cells exposed to selenomethionie have shown  a  3 — fold  increase  in P53 activity.



https://www.youtube.com/watch?v=2_eLJZ8mHow

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