Since we find ourselves at least on the Northern hemisphere in the midst of the high season of flus and upper respiratory tract infections, I thought that this is exactly the time to talk about infections and their standard treatment with the antibiotics. In my opinion this topic and its many discourses entangled with it leave us behind with a lot of misconceptions, uncertainty and ignorance. Antibiotics resistant species and strains of bacteria became one of the major threats in curing infections in the hospital environment, and are spreading into the communities, examples are tuberculosis and Staphylococci infections, Escherichia coli, Salmonella enterica, and Klebsiella pneumoniae.
The following article picks up some interesting aspects of the very recent scientific knowledge, only in brief and only in fragments, because the topic is huge, and can easily fill books’ pages. I want to outline the current status quo and future visions based on todays views. This should be our concern, because each of us could one day be a victim of this development.

In community medicine antibiotics are still the quick and easy fix

Even though, it seems that the awareness of the dangerous development of treatment resistant bugs is wide-spread, and talked about a lot by physicians, biologists and media, reality reflects otherwise. Whenever a physician feels insecure about a patient’s symptoms that he assumes are related to a microorganism antibiotics are in quick and close reach. A sore throat, a severe cough lasting for some days, and here we go, the prescription for an antibiotic is quickly written, and doctor as well as patient feel safe.
Patients nowadays are not patient enough anymore to give the body the time for healing. This is of course not only their fault. Our fast moving society often doesn’t allow us to stay home for a week, the time it mostly needs to recover from an acute (in most cases virus) infection. The ability to assess the risk, the ability to interpret body signs and take action accordingly got lost in many ways. Fever turned into a phenomenon that scares people, lungs became scary monsters that people are afraid may affect the heart. Joint pains may be suspicious of a rheumatic disease etc. etc…
Unfortunately, the knowledge our ancestors about what to do in cases of acute infections got almost lost. Moreover, many of us prefer to hand over the responsibility to the doctor.
Therefore we go and see the doctor for illnesses that usually disappear by itself and don’t need medical treatment. At the doctor’s two fears collide. Ours, we don’t want to die and the doctor’s, he doesn’t want to make a mistake and disappoint the patient or even get sued. In this setting antibiotics became a quick and efficient fix.

The dilemma starts where antibiotics are not seen as chemical compounds that are active in a bacterium within a body and an environment

There is a profound misconception here. Therefore let’s put the definition antibiotic at the very beginning of this article. Any class of organic molecule that inhibits or kills microbes by specific interactions with bacterial targets, without any consideration of the source of the particular compound or class can be called an antibiotic. Thus, purely synthetic therapeutics are considered antibiotics.
The meaning of the word changed over the decades. Today common sense connects antibiotics and its meaning with an agent that is ridding us of bugs of all kinds. Back in the days of their discovery the term antibiotics simply described its use, its laboratory effect, or its activity as a chemical compound. The term antibiotic does not say anything about its mechanism of action.
Unfortunately, due to ignorance and fear antibiotics are administered neglecting its mode of function and its effects within the bacteria, the body and the environment. The interactions of the antibiotic, the targeted microorganism and the body are not part of the medical discourse between patient and doctor. The problem of the development of resistant strains is located somewhere outside, far away from the individual situation of the patient. Antibiotics are basically for the good of the patient. Rarely we are aware of the fact that these compounds are actively spread in our environment with the detrimental consequences of resistant bacteria and the emergence of a bacterial monoculture destroying the healthy balance of microbial diversity.
Antibiotics became an unquestioned therapeutic fact. The harmful sides of this medication seem to me to be a discourse that became completely disconnected from the patient’s and doctor’s actual therapeutic interactive environment.

Antibiotics interact with the metabolic pathways of bacteria while viruses interact with the cell and don’t respond to antibiotics

At this point we are right in the center of the misunderstanding. Far too many antibiotics are prescribed without differentiating between viral and bacterial infections. Antibiotics cannot interact with viruses, because viruses don’t have an apparatus for the biosynthesis of the molecules the antibiotics interact with. The virus needs a host’s cell to do this job for it. Viruses integrate themselves into a living cell. They can do this on many levels from the nucleus to the cell, to its membrane. The virus and its metabolites can take over the control of the cell and its metabolism, and change the cell’s dedicated function. Viruses replicate by using the cell synthesis machinery, then virus metabolites and viruses spill an organ, an organ system, or the whole body. An acute virus infection may be the apparent phenomenon.
Or, the virus does not succeed to conquer the cell immediately, but silently integrates itself into the cell, and may finally induce a mutation in the nucleus or a change in one of the many signaling pathways of the cell. This mutation or change can lead to optimizing the cell functions or it can on the long run be deleterious for the cell, the organ or the organism by inducing a chronic virus infection or contributing to the emergence of a tumor.

Bacteria are not good or bad per se, nor is hygiene, we need to see the environment

Now, back to the antibiotics that are intervening with the biochemical pathways of the bacteria. To understand the many problems we face today due to the irresponsible use of antibiotics we have to have a rough idea how bacteria tick and survive on this globes for trillions of years. Men and bacteria coexist in a symbiotic way ever since. Our gut contains more bacteria (more than 500 species identified until today) than our body cells, and there are other mucosal linings colonized with bacteria that play an integral part in keeping our body in balance. Everybody got his or her very own microbial ecosystem. This means that my gut’s E. coli which is non-pathogenic for me, may induce an illness in you.
Thus bacteria play an essential role in our well-being. They may even be at the very beginning of more complex life, when cell fusions finally lead to complex organisms. Recent research discovered receptors on human cells that are either identical with bacterial elements or exactly mirror bacteria. These receptors make an essential part of our innate immune system by identifying bacterial components. It is well known today that our immune system displays patterns of receptors on immune cells that are able to recognize all common species of bacteria. This was a very brief outline of the positive aspects of bacteria, and now the negative ones, when bacteria turn against us.

Bacteria became almost synonymous for evil and dirty. This is not amazing if we go back in history when thousands of people died from bacterial infections often in their very early years. We thought to have solved this problem after having discovered antibiotics. Everybody knows that this was not the case, and if we don’t take care, we may even fall back into the pre-antibiotic era.
Here it is the double-edged sword: hygiene was one of the biggest steps forward in making our health care systems working successfully, on the other hand this same hygiene is turning against us. The soil’s and the air’s microbial ecosystem drifted out of balance. The balance among the many species and strains of bacteria controlling and constraining each other went berserk. Like in our flora we push the world of bacteria from diversity to monoculture. One phenomenon is the emergence of antibiotic resistant bacteria strains and species, another may be the increase in allergies and autoimmune diseases (another topic, another article!).

The realm of bacteria is a tightly interwoven communication network

The bacteria and their organizational principal accounts for many of the issues we have with antibiotics. We could have known better much earlier if our distortion field had not been so rigid. Only in the past few years has it been appreciated that gene exchange is a universal property of bacteria that has occurred throughout eons of microbial evolution. As mentioned already above the discovery of bacterial gene materials in the nucleus of cells including those of humans gives strong evidence about the great importance of horizontal gene transfer in the evolution of the genome on the one hand, and the organization of the bacterial collective on the other.
The way bacteria are communicating with each other, how they are able to exchange genetic materials, and the fact that they are producing antibiotics and express antibiotic resistant genes themselves indicates that the problem of resistance is integral part of the problem when dealing with bacteria and antibiotics.
Obviously resistance was always there, perhaps it is a question of survival for bacteria.

Accelerated emergence of resistance is the downside of one of the most valuable discoveries of mankind

Penicillin was discovered by Alexander Fleming in 1928, and in 1940, several years before the introduction of penicillin as a therapeutic, a bacterial penicillinase was already identified. Once the antibiotic was used widely, resistant strains capable of inactivating the drug spread. This phenomenon kicked off huge research efforts to find other compound that may evade cleavage by penicillinases. Only now, knowing what we know makes us appreciate and assess the value of the identification of a bacterial penicillinase before the use of the antibiotic. Recent findings confirm that a large number of antibiotic resistant genes are components of natural microbial populations. Are antibiotics and resistance an inseparable couple?

Let’s have a more closer look on these small creatures. Let’s not forget that they are alive and herewith possess their own genome and their own metabolic system that produces and secretes a large number of molecules, molecules of which we know only very little about. Bacteria possess pumping systems that prevent intracellular accumulation of molecules that may be able to kill or freeze them. The coexistence of synthesis and resistance functions in one and the same bacterium has been confirmed in recent studies. It seems logic to us that resistance is a mechanism of protection, an element of the bacterium that is needed for its chemical equilibrium.

It is a completely different story to look at bacterial monocultures in a lab or at bacteria in the wild

Only recently scientists started to study microbes in their natural environments. And it occurred what usually occurs when you leave the lab and have a glimpse on nature: you change your mindset and then your working hypothesis, and so it happened to the scientists observing bacteria in the wild.
They saw the large number of bioactive microbial compounds they produce, and found a lot of open questions they try to find the answers for now. Antibiotic activity was only one of the biological properties of the many bioactive small molecules. They exhibit extensive multi-functionality and most likely are involved in cell-cell signaling within and among the network of bacteria and other organisms in the environment (fungi, plants, insects, and even human and animal hosts). Researchers changed their path while investigating the interactions within complex bacterial communities (microbiomes) in different environments. They realized that many diseases occur as the result of polymicrobial infections, and they are working now on the implications of these observations.

If we look at the so-called resistance mechanisms from the standpoint of an antibiotic that lost its effects resistance gets a negative flavor. If we look at it from the perspective of a bacterium the process of “resistance” may facilitate cell-cell interactions, protect natural degradation pathways, or other functions we don’t know yet.

Some scary examples that should make us think when to use antibiotics or please, no antibiotics in cases of flu and common cold

Erythromycin was an early example. It was introduced as an alternative to penicillin for the treatment of Staphylococcus aureus in Boston City Hospital in the early 1950s. It was completely withdrawn after less than a year because 70% of all the S. aureus isolates were found to have become erythromycin resistant. The same was observed with a tetracycline and chloramphenicol and, subsequently, with other antibiotics.
Unfortunately, the colossal need for these valuable drugs has had a significant environmental downside. In the 60 years since their introduction, millions of metric tons of antibiotics have been produced and employed for a wide variety of purposes. Improvements in production have provided increasingly less expensive compounds that encourage nonprescription and off-label uses. The cost of the oldest and most frequently used antibiotics is (probably) mainly in the packaging, and this is really ironic if we look back in history when pandemic infections stroke mankind.

What happened during the evolution of bacteria over several billions of years cannot be compared to the phenomenon of antibiotic resistance development and transfer over the last century. The existing processes of gene acquisition, transfer, modification, and expression that were in place ever since are expanding and accelerating in the modern biosphere. The way how bacteria exchange genes (plasmids, phages, and transformation) are well known from the lab. But in the natural environment other processes may exist. For example, bacterial cell-cell fusion might be favored in complex mixed microbial communities.
Another important point, we don’t know the pathway from an environmental gene to a clinical resistant gene yet. We can only assume that this road is easy to walk on for those genes.
One more practical remark for you if you have to take antibiotics: Especially at sub-inhibitory concentrations, the process of antibiotic resistance development may be facilitated.

What could be done to slow down the detrimental signs of resistance development?

Over the years, many different solutions have been proposed by experts and all the major international health groups (e.g., WHO and the CDC). Among the proposals for action are strict controls on antibiotic use by humans. Here we clearly enter the territory of politics. I intentionally stay out of this area because here discussions never end, and the various agendas get blurry and disarrayed. I cannot contribute anything of influence that would really matter on a larger scale. I may only dare to advise you to question yourself before using antibiotics, and question it, if you feel the prescription was a doctor’s quick and easy pick.

Most infections are first of all viral origin, then antibiotics are not justified. If you come down with an acute virus infections it takes you up to one week to recover. Fever shouldn’t scare you. A healthy circulatory system can easily cope with 39°C and a heart frequency over 100 beats for a week or even more. Homespun remedies are not part of this article, but play an important role. We should definitely rediscover and learn about the remedies of our ancestors.
If it comes to non-antibiotic approaches for the treatment of bacterial diseases, Biestmilch is a serious option stimulating or recruiting the innate immune system of the host. Recent advances in our understanding of the roles of the human gut microbiome in innate immunity underscore the role of Biestmilch as an other therapeutic option. At least you should consider taking it together with antibiotics. The debris antibiotics leave behind has to be cleaned up by the immune system. Biestmilch empowers the immune system to do so more effectively.

This is the end of a fragment on a very complex topic.

Literature
Hawkey PM, Jones AM: The changing epidemiology of resistance. Journal of Antimicrobial Chemotherapy, 64: Suppl.1, i3–i10, 2009
Davies J,  Davies D: .Origins and Evolution of Antibiotic Resistance. Microbiol. Mol. Biol. Rev. 74(3):417, 2010
Levy St B, Marshall B: Antibacterial resistance worldwide: causes, challenges and responses. Nature supplement, 10(12): 122-129, 2004

The colostrum study I attached here suggests that Biestmilch/colostrum is superiour to the vaccines in preventing a flu.

Are you convinced? If yes, here is the promo code FLUBM-111 with a 10% deduction for our “Biestmilch against Flu” Special. >>> USA store; >>> Europe Store

The best tumor therapy is prevention

Because most cancers develop slowly over decades, prevention should stand in first place today. By prevention, we mean influencing the environment of the genetically altered cell. Prevention comprises healthy and good quality food. Eating is the most important environment modulator, closely followed by regular exercise, i.e. sport, because physical exercise activates the immune system and suppresses inflammatory processes that are smoldering in the body. It is also very important to not eat too much, i.e. restrict calories.

Biestmilch belongs to the food plan (it is a foodstuff). It is a kind of immune serum, a substance that is able to calm down chronic inflammatory tissue.

Biestmilch can modulate the inflammatory environment of the tumor

The inflammatory response should actually contribute towards removing the tumor cells. However, in the case of humans with tumors, the inflammatory response is unproductive. Inflammatory and anti-inflammatory processes are no longer in balance but have displaced towards the chronic inflammation. It is typical for the environment of the tumor that receptors become insensitive meaning no effective anti-tumor response is generated.

Today, the therapeutic challenge principally lies in normalizing the deregulated inflammatory network in such a way that the result is a regular moderate inflammatory response. Thanks to its diversity, Biestmilch as one of the very few substances available has this potential. Furthermore, it can stabilize the immune system for chemotherapy to such an extent that subsequent metastasizing may be delayed or even prevented, and side-effects of the immunosuppressant treatment mitigated.

How to take Biestmilch:

You should take Biestmilch every day. Make it part of your food plan. You don’t interrupt the intake.

Take 900 mg every day. If you are taking Biestmilch as preparation for chemotherapy or in addition to that, increase the amount to 3 x 900 mg every day. After chemotherapy reduce step by step to 900 mg or 600 mg. In the case of a repeat chemo-cycle, please increase the dosage again to 3 x 900 mg.

1
One hypothesis reads as follows: The cell reveals a gene defect that can no longer be repaired. For this reason, the external appearance of the cell deviates from that of the normal cell. Such a cell no longer divides itself up asymmetrically into a cell with a function (effector cell), which depends upon which organ or apparatus it is allocated to and into a stem cell but symmetrically into two cells with functions. Yet, it is not a tumor cell. As long as the environment surrounding the cell suppresses cell proliferation, a tumor does not develop.

2
If, however, a carcinogen or a chronically inflamed environment affects the cell to the extent that the brake preventing cell proliferation is released, then the cell begins to proliferate in an uncontrolled manner. The result is a mass of cells such as polyps in the colon or papilloma in the skin. For a so-called malignant tumor to develop, a number of additional genetic or cellular changes must occur. It’s not until now that the step towards the tumor becoming malignant follows.

3
Another hypothesis – worded by Potter back in 1978 – explains the emergence of a tumor as being a blockage of cell development on their way from the stem cell to the cell that is equipped with the function determined for that cell. These cells still carry a large number of options for developing into the various effector cells. An interruption to this development can happen at any stage of this process. Influences from the cell’s environment can speed up cell division and prevent the normal death of the cell.

4
You have probably often come across the term oncogene. More than 100 oncogenes have already been identified. Oncogenes are DNA parts that serve as the template for the synthesis of protein substances with differing tasks like growth factors, receptors, signal-transferring molecules.

5
The tumor suppressor genes have a quasi contrary task to the oncogenes. They form the template for the growth of inhibitive factors such as bridging molecules. These are structural proteins between cell membranes forming channels for the direct transfer of small molecules and ions between the cells. These bridging molecules are central structures of monitoring growth and cell differentiation. If a cell with  such a defect gene has still got bridging connections, it is able to develop in its target cell to a certain extent. Its direct contact to the other cells in the network inhibits uncontrolled proliferation.

In tumors, the bridging molecules are usually missing. That means that the cell loses an important component for its interaction with the environment. An activated oncogene and an inactivated suppressor gene can permanently stimulate growth.

The objective of the research is to make tumor treatment that is currently very poor more specific and targeted.

For references and more on tumor development in specific, please read part one.

10 years of experience allow us to say that Biestmilch is a powerful tool in the treatment of cancer. Immune and inflammatory parameters return back to normal. CD4/CD8 ratio normalizes. Side-effects of chemotherapy are far less pronounced in many cases. This comprises hair loss, nausea, gut issues, mood swings etc.

Here, you can find texts I wrote about this natural remedy that in my opinion cannot be topped when it comes to the strength and diversity of its effect. Biestmilch is not harmful to you, doesn’t hurt you. In order to understand Biestmilch, you will have to say goodbye to conventional ways of thinking. There’s no need to distance yourself from scientific knowledge but you do have to move along the borders of science where rethinking takes place and new things come to life.

Part I
Tumor – See the opportunities
A tumor is not an accumulation of malignant cells

You may find that sounds like a provocation. I would now like to tell you why that is not the case and why this scientific observation uncovers great opportunities for you.
Scientists have recently recognized that the notion of a tumor consisting of an accumulation of malignant cells, which have withdrawn themselves from growth control, does not apply. This view should thus to be discarded and become history. Unfortunately, medicine has not yet it adopted.

A network of regulatory circuits controls the balance of the cells’ proliferation and differentiation

Cancer cells display defects within their regulatory circuits that control cell proliferation, balance growth and quiescence, guide regeneration and cell death. These signalling processes of maintaining the cell’s balance are complexly intertwined and can be disturbed or disrupted in many ways. This is why we can differentiate among more than 100 types and subtypes of tumors within one single organ. In other words, no one type of cancer resembles the other.
How many regulatory circuits in a target cell need to be broken that control processes cannot stop a tumor from growing anymore and whether the same or similar regulatory circuits in every tumor cell are affected in the various tumors remains unknown to this day. Which regulatory circuits in the cells run independently from the environment and which are coupled to signals from the micro-environment is likewise unexplored. Whether the large number of cancer-related genes can be tied to certain regulatory circuits also needs more research.

A genetic defect alone does not necessarily lead to a tumor developing

It can take decades for a tumor to reach the size of medical significance, i.e. until symptoms become apparent. Tumors usually grow very slowly and, in addition to that, a series of unfortunate coincidences must concur. A defect in the DNA is not sufficient to make a tumor develop and that is why a tumor is not simply a collection of malignant cells whose growth proceeds in an aggressive and uncontrolled way. And because of this fact, a suitable lifestyle that creates a healthy environment for the cell can very much help to prevent the development of a tumor.

For a tumor to start growing, a number of factors must coincide
Disorders of the cell biology can take place on the level of the cell core, the cytoplasm, the receptors, the extra-cellular matrix and the neighboring cells. The underlying processes are arranged on a time basis in 3 phases: 1) the initiation of the DNA, 2) the promotion in the intra- and extra-cellular environment and 3) the progression through tumor-specific communication processes beyond the primary tumor.
First of all, the cell experiences a genetic change, that is initiated. It can linger or pause in this state for decades on end. This means a tumor never grows. So, as you see, a genetic defect does not suffice to produce a tumor.
However, if such a cell experiences an irritation such as the influence of a carcinogen or a chronic inflammatory change to its environment, then the genetic defect may manifest in the development of a tumor. A chronic inflammatory environment gives this genetically weak cell a growth advantage over other cells.

The tumor cell grows independently by loosing contact with their neighbor cells

No normal cell can multiply itself without stimulating signals. In contrast, a tumor cell grows independently; it loses its coupling to the environment. Many oncogenes function by copying normal growth signals. Healthy cells are connected by an array of molecules called connexins.
These bridging molecules are essential for the communication among cells. In contrast pluri- or omnipotent stem cells are characterized by not carrying such connexins on their surface. Thus, they have no bridges for communicating with other cells. These bridging molecules are significantly involved in controlling the growth of cells and tissues. Communication is thus an important control process.

Characteristics of a cancer cell:
1. Self-sufficient generating its own growth signals
2. Insensitive towards signals limiting and regulating growth
3.Undermining the process of cell death (apoptosis)
4. Endless potential for proliferation
5. Maintaining the formation of vessels
6. Penetrating into the tissue and metastasizing

The cell’s environment is just as important as the cell itself

In science, one speaks of epigenetic processes, which play a central role in the development of tumors. As you know, the cell consists of the nucleus in which chromosomes, the DNA, the genetic material so to say are located, of the cytoplasm surrounding the nucleus, in which a large number of molecule assemblies form structures that are necessary for the cell to live and to become what it is and what it does. The cell as a whole is surrounded by a membrane just like the nucleus is. All structures that form this kind of cell have, on the one hand, parts which have a very flexible shape (receptors, ligands) and continuously send and receive signals. On the other hand, they fulfill certain tasks in the cell such as cell respiration or protein biosynthesis. Thus a stream of signals flows through the cell, which leads from the cell’s nucleus to the environment surrounding the cells and back. In simple terms, it is a fabric of thousands of feedback loops infinitely sending signalls from the inside to the outside and back.
The resulting signal patterns determine the specific functional state of the cell. Irrespective of what function a cell has, in principle, all cells work according to the same principle.

Working in basically the same way a cell is susceptible to change either for the good or the bad on various levels in terms of  place and time.
Cell growth is thus not a phenomenon that is controlled solely by the cell’s nucleus and its genetic material. The cell is closely connected to its environment, exchange is narrow and intensive. Not only do signals/impulses/messages from the interior of the cell reach the cell’s surroundings, thus changing the cell’s state, but signals/impulses/messages from the environment likewise influence the cell’s and the nucleus function and activity. In this way, the cells and the space among them form an entity of brisk exchange.

Tumors only develop in chronic inflammatory environments

Virchow saw a correlation between inflammation and tumor back in 1863. Ever since, research has been changing in such a way that can barely be compared to those times. And yet, this postulate gained more relevance than ever. In the meantime we know from some chronic viral infections that they can make the way for tumors to develop. And the same applies to chronic inflammations like rheumatism or chronic inflammatory bowel diseases.
Inflammations are usually self-limiting processes. With a fine-tuned immune response, the immune system makes sure that inflammatory and anti-inflammatory processes are balanced and ultimately lead to healing.

Tumor patients display a weakened (suppressed) immunity. When a tumor starts to grow or metastasize, then it has usually already undermined the immune system with its monitoring strategies. An intact immune system patrols the body and removes the cells that are no longer behaving properly.
Dvorak recognized the similarities between wound healing and tumors back in 1986. In contrast to a tumor, a wound heals itself. In a tumor, the process continues by factors being released unremittingly, which maintain the inflammation. As is the case with wound healing, the formation of vessels for a tumor to emerge plays is crucial, for a tumor that measures more than one to two millimeters, blood vessels are vital.

To put it a nutshell:

In order for a malignant tumor to start growing, an external or internal trigger, an inflamed environment and some damage to the DNA must concur. An improbable event for an individual? Many malignant tumors are triggered off by infections. A history of infection can be assigned to more than 15% of all tumors worldwide; that is more than 1.2 million cases a year. Thus, tumors develop as the result of a multi-leveled process, which leads from an initial benign change of the cells to an invasive and then metastasizing disease. This process takes many years until it has fully developed. The long period this process requires strongly implies that it has to assert itself against a background of strict and diversified control processes that are supposed to prevent anarchical cell behavior.

It is thus probable that a certain environment tied to a genetic disposition changes the cells to such an extent that they become more receptive for endogenous and exogenous carcinogenic influences. It may depend on whether the carcinogens can actually trigger off tumor growth and how long it takes until the process is clinically apparent.

If you want to know more about the hypotheses scientists are currently working with, please read part II of the article, part III gives you some guidelines on how you can administer Biestmilch in tumor patients.

Sources of literature
Coussens LM, Werb Z: Inflammation and cancer. Nature, 420: 860 – 867, 2002.
O‘Byrne KJ, Dalgleish AG: Chronic activation and inflammation as cause of malignancy.
British Journal of Cancer, 85 (4): 473 – 483, 2001
Shamgar B-E: The promotion of tumor metastasis by surgery and stress: immunological basis and implications for psychoneuroimmunology. Brain, Behaviour and Immunitiy, 17: 27 – 36, 2003
Lotem J, Sachs L: Epigenetics wins over genetics: induction of differentation in tumor cells.
Cancer Biology, 12: 339 – 346, 2002
Trosko JE: The role of stem cells and gap junctional intercellular communication in caringenesis. Journal 
of Biochemistry and Molecular Biology, 36 (1): 
43 – 48, 2003
Trosko JE: Chang CH-Ch, Upham BL, et al.: 
Ignored hallmarks of carcinogenesis: stem cells and cell-cell communication. Ann. N.Y. Acad. Sci., 1028: 192 – 201, 2004
Hanahan D, Weinberg RA: The hallmarks of cancer. Cell, 100: 57 – 70, 2000

Jet lag or travel fatigue

Travelling as such is related with fatigue symptoms and problems of adaptation which are not necessarily due to jet lag. The term jet lag per definition describes health issues that occur after you have been crossing several time zones. Travelling as such causes regulatory disturbances of your body even without jet lag. You certainly have experienced these feelings of discomfort due to functional dysregulations. Common are sleep disturbances, gut and stomach issues, head ache, mood swings, weak performance, common colds or other infections due to the travelling stress caused by dysfunctions of your stress coping system and your immunity. After one or two nights of good sleep these problems slowly subside. Then you have fully arrived at destination.
With jet lag that’s different, and it is again different whether your travel is east or westbound.

Some science behind the jet lag – we are a diurnal species

Jet lag is defined as a circadian desynchrony, a disruption of the harmonic entanglement with our environment. Our body functions are tightly coordinated over time, each cell, each organ has got its own clock that is overall coordinated by a nucleus in the brain (supra-chiasmatic nuclei of the hypothalamus, SCN), at least that is what is known until today. The basic rhythm is approximately circadian (24 hours), with of course an individual variability of several minutes. Biological circadian rhythms are internally generated. They even persist in the absence of time cues such as alternating light and darkness. Individuals kept in a time free environment (or at least with very weak time cues), manifest their own endogenous periodicity – ‘free-running’, an inherited characteristic. Removal of the SCN in mammals leads to the loss of virtually all circadian rhythms.
The mismatch between the timing of the internal circadian clocks and the external environment causes a pattern discomfort that is called jet lag. After time zone changes the circadian system adapts slowly to realign with the new schedule, approximately one day for each hour of time zone change, faster westwards, with different components of the system adapting at different rates (internal desynchrony).
The perceived manifestations vary from one individual to another, with number of time zones crossed, with direction and timing of flights and probably with seasons. However, the major complaints are poor sleep, daytime fatigue and poor performance. Travelling eastwards, short sleep and long sleep latency are common, travelling westward short sleep and early wake up are manifest. Poor alertness and fatigue during daytime are attributed partly to a lack of sleep that accompanies most travelling and partly to the concomitant presence of night time rhythm physiology. Under circumstances you are perfectly rhythmized your nightly core body temperature is low, so are alertness and performance, metabolism is in build-up mode and melatonin secretion peaks.

There are possible long term consequences of frequent desynchrony as evidenced by epidemiological and animal studies. These include cognitive deficits, gastrointestinal problems, increased risk of cancer, infertility and heart disease. However, not all reports are consistent. Adapting to phase shift becomes harder as we grow older for uncertain reasons. Moreover the genetic background influences our adaptation abilities. Various polymorphisms have been identified in human clock genes and associations are evident with phenotypic characteristics such as diurnal preference, vulnerability to disease and probably rate of adaptation to phase shift.

What can we do to facilitate the adaptation process

Jet lag is a problem for most time zone travellers, affecting sleep, performance and may possibly have long-term health consequences for certain individuals (see genetic background). It is due to the misalignment of the internal circadian clock(s) with external time cues. For short stopovers (1–2 days) it is advisable not to try and adapt but to schedule critical activities to daytime in the departure time zone and maintain alertness and sleep by short- term measures such as a real good nap, caffeine and short acting hypnotics. For intermediate length stays (3–5 days) it would be optimal to plan activities in an intermediate phase between the departure and destination time zone. The circadian peak is right within the sleep period at destination. This could be a solution to the problem, but honestly is quite unrealistic to achieve.
For long stays in the destination time zone (more than 4–5 days) strategies to hasten adaptation can be employed. These include timed exposure to light of suitable spectral composition and intensity (natural bright light when this can be appropriately timed is best, but will be dependent on season in temperate zones). The American Academy of Sleep Medicine recommends the timed use of the chronobiotic melatonin to shorten adaptation. Melatonin itself is now available in Europe on prescription and melatonin agonists are becoming available. The use of both light and melatonin requires careful attention to timing and, in the case of light, of avoidance as well as exposure. The maximum efficacy for jet lag avoidance is by pre-flight adaptation, however, this requires time and commitment.

Summary

Travel fatigue abates by the next day, if travellers succeed to have a good night’s sleep; jet lag after eastward flights lasts for several days roughly equal to two-thirds of the number of time zones crossed and about half the number of time zones crossed after westward flights. Again, there are obvious differences between individuals. To hasten adaptation would be a great achievement, but is tricky and time-consuming. Many of us don’t have this time due to their restricted holiday time or their jobs’ pressure.
Caffeine and short acting hypnotics, light exposure and melatonin again at the right time of the circadian shift between departure and destination, enough sleep, light and healthy food to avoid stress on stomach, gut and immune system, all of them closely related and easily affected by long-distance travelling are options to make it easier to adapt to a new time zone.

Ref.
Arendt J: Managing jet lag: Some of the problems and possible new solutions. Sleep Medicine Reviews 13, 249–256, 2009
Waterhouse J, Reilly Th, Atkinson G, Edwards B: Jet lag: trends and coping strategies. Lancet, 369: 1117–29, 2007

This survey is closed.

This survey closes on Sept. 13, 2011

Do different sports need distinct tapering strategies?

We don’t know yet. A lot of science work has still to be done to give the various taper strategies a scientific background.
Scientific studies need to outline a proper hypothesis, and consider the complexity of the physiology behind. Until today we don’t even know whether the taper has to change depending on the sports. Maybe we have to discriminate between strength and power sports, endurance and ultra-endurance sports, maybe we have to look at the individual.
That our knowledge about tapering is still very limited, has in my opinion got mainly two reasons. One is, science studying this field is still very young. The first scientific study was reported as recently as 1992 (Shepley at al.). Secondly, the studies that have been performed are only vaguely aware of the complexity of the physiology behind the body’s regulatory and adaptation processes in the tapering and the preceding training. Therefore future investigations of a more dynamic nature are needed, investigations, that take the course of time of physiological changes into considerations.
Interesting to know is that round about 50 years ago we have not even been aware of the fact, that a special recovery regimen before a competition can improve performance. Training was continued right through to the competition. So it happened that guys were running a marathon before racing the marathon. One of the first authors to discuss the importance of resting before competition was Stampfl in 1955. He insisted that his distance athletes rested for full four days before competition. The term tapering was first coined by Carilie and Frank Cotton in 1947.

There are various tapering strategies around that differ in duration and intensity. Banister et al. published a paper in 1999 looking at three different tapering strategies. I think this paper is still the foundation of what is roughly done until today with lots of minimal variations and individualizations by coaches and athletes. The study by Banister found that the more rapidly you reduce training in the taper, the better is your racing performance. Thus the most effective taper was one in which training was reduced by 50% on the third day of the taper and 75% on the sixth day with a continuing reduction for the next eight days.

Is tapering a period of time for the body and the brain to adapt and recuperate?

The answer is maybe. How to measure, how to assess your very own and optimal way of tapering to achieve what seems to be clear cut: Tapering produces a dramatic improvement of performance, if you do it accordingly.
You may not be able to go for all the different and then anyway inconclusive parameters such as metabolic changes, muscle glycogen concentration, VO2max and lactate (levels that seem not be influenced by the tapering anyway). But you have access to your own mood state, sleep pattern and perception of exertion. All three are complex physiological and psychological phemomena that indicate your condition and well-being as a whole. It is the body and the brain, both together fresh and ready to rock that make up for a peak performance. All three are emergent states that indicate the condition of your immune system, your ability to cope with stress factors and adapt to changes etc. If during the taper your mood (e. g. perceived fatigue, depression, anger, confusion) is not getting better, your sleep not more restorative and your level of vigour not higher, then there was probably something wrong with the preceding training. At least these are the conclusions I draw from the incoherent literature I read.

Is tapering a phase for focusing on neuromuscular recruitment?

Let’s dare to say yes to this point, one of the few with almost unanimous consensus among the scientific community. Taper results in an increased strength and power output in athletes obviously regardless to the sports they do. As I would put it, during the taper  you have to rest, but the current of signals from the brain to the periphery and back should not stop. This is at least what field experience of athletes proves. Signals have to be sent with sufficient intensity and frequency to keep open all the paths from the brain to the periphery of the muscles and other organs and back, to have all the necessary neurones on stand-by mode and ready to fire when receiving the command of the race’s starting signal.

Summary

Scientific evidence confirms that tapering produces a dramatic improvement of performance. The effect is greatest if there is a rapid reduction in training volume already in the first few days of the taper and if training during the taper is at high intensity, approximating 5-km race pace for runners.
To sharpen the training to optimize the training effects on the brain, and its ability to recruit a larger muscle mass for longer during subsequent exercise, and at the same time to leave enough time for adaptation and recuperation that’s what I think counts during tapering.
The key could be to do very little training during taper, but to train only at race pace. Tim Noakes’ expresses it like this: »Once you decide to taper, do as little training as your mind will allow, but do this little training at fast pace.«

Many of you have been receiving race packages during the last months in return for taking little biests on the road and through races. Therefore we once again want to outline what the booster actually is and how you can take it to get the optimum out of it.  And please, read about the experiences our Biest Athletes have made with the Biest Booster!

Product development

Hard to believe but true, the BIEST BOOSTER is a high-tech product even though it is also a truly natural product. Biestmilch is natural through and through and so are the 100 mg of caffeine contained in the Booster. They originate from the natural caffeine extract of the guarana fruit. The Booster’s matrix is composed of a dextrose derivative called Emdex®. So in the end, what makes the Booster a high-tech product, is the art of combining 4 grams of Biestmilch with 500 mg of Guarana extract into an edible small shape.

BIEST BOOSTER and its bitter taste of healthiness

The idea of designing a product that may be able to facilitate the a breakthrough for Biestmilch, had been on our minds for quite some time. Even back in the first days of Biestmilch back in the year 2000, we had thought a product that would able to generate instant gratification for our customer, while Biestmilch regular takes 10 days up to round about 3 weeks to kick in.
After a couple of years of experience we decided to take up the idea of »a product for the impatient« again. We knew enough about Biestmilch and its efficacy to finally dare to develop such a product.

We knew that 4 grams of Biestmilch lift the spirits and help to improve the general well-being under the various conditions such as issues with immunity. Guarana is well known to you as a natural caffeine extract and stimulant supporting cognition. Now the basic idea was there and along with it the problems that usually emerge, when moving from theory to reality. All of a sudden the Biestmilch powder put up some resistance. So did the sorbitol, shape, structure, taste, solubility, brittleness and stability… a number of various problems suddenly popped up and put our theoretical concept to the test.

How to put 4 grams of Biestmilch into an edible shape?

In April 2006 we developed granules, which were neither edible nor possible to swallow in the respective amount. It foamed and frothed inside the mouth in a strange manner and gave any observer a hearty laugh.
As we already had some experience with developing bars, the next test product was a bar with 4 grams of Biestmilch and 500 mg of Guarana. The tiny Biest Booster bar was finished by June 2006. It tasted of bitter orange and was a bit hard, but we quite liked the taste. I am afraid to add, that we remained the only people with this opinion.

A chocolate coating gave the Booster a tastefulness that threatened the healthy aspects of our product. To much guarana may induce flushes, headache and restlessness. We took a step back from this kind of Booster. Another reason to distance ourselves from the bar was that we would then be compared with the gigantic market of bars. But the Booster is unique and incomparable, so we moved to the next testing phase.
In September ’06 we had made it to the first tablet, a square block. It was based on a sorbitol matrix. Because of its laxative effect, if consumed in large amounts, sorbitol was not exactly an option. And sorbitol has a rather narrow bandwidth concerning stability and consistency. Once the machine was even run down, because the block was simply too thick and the sorbitol jammed the machine’s extruder. So we had rock hard bricks, with which one could have very well killed somebody.

Back to re-thinking and testing

This thinking and testing process resulted in the first octagon version. The experiments lasted from February till April 2007. A huge breakthrough for the Booster development was the choice of the matrix Emdex® instead of sorbitol. Emdex® is a very modern dextrose derivative and a far better matrix than sorbitol. Taste and feeling in the mouth were improved greatly. At last, after a series of 8 to 10 different kinds we ended up with a product that could be considered for a broader range of testing. We still had massive problems with the stability of the tablet when trying to pack it. The octagon constantly broke into two pieces when put into the side sealed bag.

When eating the 7,8 g heavy Booster we also still had the problem of a kind of »suffocating sensation« and taste of mouth.

Series 11 brought the final breakthrough

Instead of Biestmilch powder we used agglomerated colostrum. In this testing series all of a sudden the Booster was stable and good to chew. Series 11.1 and 11.2 were mere variations in taste and mouth feeling to optimize »edibility«. With the Booster 11.2.4 the final decision was made for marketing the product. A first production of 4200 pieces left the factory in August 2007.

Since then we have been fine-tuning still, and worked on the mouth feeling. All the years that passed by until today show that those who once tried the BIest Booster and felt the instant positive effects become loyal consumers.
Therefore embrace the slight bitterness of its taste, and enjoy chewing it. After all the sweet gels and bars you eat, the Booster can even be a relief for your gustatory sense.

Guaraná – a slow-release caffeine stimulant

Guarana from the Portuguese guaraná (Paullinia cupana) is a climbing plant in the maple family, native to the Amazon basin and especially common in Brazil. Guarana features large leaves and clusters of flowers, and is best known for its fruit, which is about the size of a coffee bean. As a dietary supplement, guarana is an effective stimulant. It contains about twice the caffeine found in coffee beans (about 2–4.5% caffeine in guarana seeds compared to 1–2% for coffee beans). Compared to the caffeine from coffee beans caffeine in guarana is slowlier released and is therefore active between 4 to 6 hours.
As guarana is rich in caffeine, it is of interest for its potential effects on cognition. In rats, guarana increased memory retention and physical endurance when compared with a placebo. A 2007 human pilot study assessed acute behavioral effects of guarana extract. Memory, alertness and mood were increased confirming previous results of cognitive improvement following the consumption of guarana.

Products with natural caffeine content

• a cup of coffee (150 ml) contains ca. 30 to 100 mg a small Espresso (30 ml) ca. 40 mg caffeine.

• a cup of black tea contains an average of 50 mg

In former days the caffeine in tea leaves was called theine, chemically its exactly the same as the caffeine in coffee. Only 100 g of dried tea leaves contain more caffeine than the same amount of roasted coffee beans.

• Guarana contains 4 to 9 g caffeine per 100 g dried weight.

• Cacao contains with 6 mg per cup a little bit of caffeine, but mainly theobromine.

• Chocolate contains caffeine as well (milk chokolate ca. 15 mg/100 g, bitter choclate ca. 90 mg/100 g), moreover theobromine and other stimulant substances.