Serving all of Southwest Forida. Call today for FREE Medical Exam & Consultation. 239-596-8886

What Is Bro-Tox and is it Safe?

What Is Bro-Tox and is it Safe?

Dear Doctor,
My girlfriend gets Botox regularly to eliminate wrinkles, and she wants me to get Botox too.  I have heard some horror stories about Botox… and the idea of putting a poison in my forehead has me concerned.  Could you give me some history on what exactly this substance is, where it comes from, what it actually does to you…and is it safe?  Thank you in advance!

Tim
Naples, FL.

Thank you for the question Tim.  I understand your concern… the thought of injecting a “toxin” into the body scares a lot of guys, however we are seeing a lot of men embrace the idea of obtaining a more youthful appearance by using this treatment.  Women have embraced the use of Botox for years and it has become the go-to procedure to reduce or even eliminate lines and wrinkles on the face and hands, giving the skin a smooth and more youthful look.  When men use Botox or the equivalent products, it is often referred to tongue-in-cheek as “Bro-Tox”.  Treatments can erase years off a man’s face by eliminating lines that make us look old.

The goal of my response is to give you more information than is typically found “on-line”… so that you can make an informed decision on whether you want to try this treatment, and so that you will look even smarter at the next cocktail party.

“Bro-Tox”, or Botulinum Toxin Type A, commonly branded as Xeomin or Botox, is pharmaceutical grade botulinum toxin used for medical and aesthetic procedures.  The injection of botulinum toxin A is the most common cosmetic procedure performed on men and women today.  These medications are derived and refined from a neurotoxic protein produced by the bacterium Clostridium botulinum.  This microbe is responsible for a type of often deadly food poisoning called “botulism”.  If infected by the bacterium, the botulinum toxin prevents the release of the neurotransmitter acetylcholine, which cause muscles to contract from nerves ending at the neuromuscular junction and thus can cause flaccid or limp paralysis. (*More technical information can be found at the end of this response.)

In 1820, Justinus Kerner, a small-town German medical officer, gave the first complete description of clinical botulism based on extensive clinical observations of what he called “sausage poisoning”.  Following experiments on animals as well as on himself, he concluded that the toxin acts by interrupting signal transmission in the somatic and autonomic motor systems, without affecting sensory signals or mental functions.

He observed that the toxin develops under anaerobic (without oxygen) conditions, and can be lethal in very small doses.  His foresight in suggesting that the toxin might be used therapeutically earns him recognition as the pioneer of modern botulinum toxin therapy.

Seventy-five years later, in 1895, Émile van Ermengem, professor of bacteriology correctly described Clostridium botulinum as the bacterial source of the toxin.
Van Ermengem was able to do this after several funeral attendees were poisoned by eating partially salted ham.  He fed an extract of that ham to lab animals and found it to cause botulism-like paralysis.  Van Ermengem then isolated and grew the bacterium, and described its toxin.  This toxin was later purified by P Tessmer Snipe and Hermann Sommer.

Over the next few decades, commercial food canning was becoming more popular and was approaching a billion-dollar-a-year industry.  Unfortunately, unbeknownst to the canning companies, poor canning practices of the time caused botulism to become a public health hazard.  Karl Friedrich Meyer, a Swiss-American veterinary scientist, developed techniques for growing the organism and extracting the toxin in order to find ways of preventing growth of the organism and its toxin production.  He found that C. botulinum was destroyed and its toxin was inactivated by heating the products in the can or jar before sealing.  The canning industry was thereby preserved and botulism was no longer a major health concern.

During World War II, weaponization of botulinum toxin was investigated.  An Army biochemist developed the concentration and crystallization techniques to create the first clinical product.  When the Army’s Chemical Corps was disbanded, several of the scientists moved to the Food Research Institute in Wisconsin, where they manufactured toxin for experimental use and generously provided it to the academic community.

A group of Ophthalmologists, led by Alan B. Scott, who specialize in strabismus, (a spastic eye muscle disorder), were very interested in the botulinum toxin.  This is because strabismus surgery frequently needed repeating and a search for non-surgical treatments using various anesthetics, alcohols, enzymes, enzyme blockers, and snake neurotoxins had already begun.  They began researching and experimenting with botulinum toxin to treat strabismus.  They developed a method of injecting botulinum toxin using EMG (electromyogram) to guide the injection.  The EMG detects electrical signals from an activated muscle.  They started by injecting botulinum toxin into monkey extraocular muscles.  The result was remarkable: a very small volume (a trillionth of a gram) induced paralysis that was confined to the target muscle, for a long duration, and without side-effects.

After working out techniques for freeze-drying, buffering with proteins, and assuring sterility, potency, and safety of the toxin, they applied to the FDA for investigational use of the drug.  They began manufacturing botulinum type A neurotoxin in a San Francisco lab and the first human strabismus patient was injected with botulinum toxin in 1977 by Scott.  Its clinical utility was reported in 1980 and soon after, Scott trained hundreds of ophthalmologists to perform the same EMG-guided injection of the drug which he named Oculinum or "eye aligner.”

In 1986, Scott's manufacturer and distributor of botulinum toxin, was unable to obtain product liability insurance and was unable to supply the drug.  As supplies dwindled the patients who had come to rely on these injections became desperate.  As the liability issues were being resolved, American patients traveled to Canadian eye centers for their injections.

Based on data from thousands of patients collected by hundreds of investigators, the drug company, Allergan received FDA approval in 1989 to market Oculinum for clinical use in the United States to treat adult strabismus and blepharospasm (abnormal contraction or twitch of the eyelid), using the trademark “Botox.”

Not long after, a plastic surgeon named Richard Clark, was the first to document a cosmetic use for botulinum toxin.  He used the botulinum toxin to treat a pateints’ forehead asymmetry caused by a left sided forehead nerve paralysis that occurred during a cosmetic facelift.  Since injured nerve can regenerate in 24 months, a two-year waiting period was necessary before definitive surgical treatment was to be performed.  He realized that botulinum toxin could be injected into the muscles of the forehead in order to smooth the wrinkles of the un-paralyzed side to match the paralyzed side.  He received FDA approval for the cosmetic use of the toxin and published the case study in 1989.

Jean and Alistair Carruthers observed that patients with blepharospasm who had received botulinum toxin injections around the eyes and upper face also had diminished facial glabellar lines.  The glabellar lines are the “frown lines” between the eyebrows.  This started the most popular cosmetic use of the toxin.  In 2002, following clinical trials, the FDA approved Botox Cosmetic, botulinum A toxin to temporarily improve the appearance of moderate-to-severe glabellar lines.

In 2000, William J. Binder reported that patients who used cosmetic injections of botulinum toxin around the face also had relief from chronic headache.  First this was thought to be an indirect effect of the reduced muscle tension but it is now known that the toxin also inhibits the release of peripheral nociceptive neurotransmitters, which suppress the central pain processing systems responsible for migraine headache.  In 2010, the FDA approved intramuscular botulinum toxin injections for the treatment of chronic migraine headache.

Botulinum toxin is now used to treat a number of disorders characterized by overactive muscles which cause spasticity or tightness.  This includes post-stroke spasticity, post-spinal cord injury spasticity, spasms of the head and neck, vagina, limbs, jaw, vocal cords, esophagus, lower urinary tract and bladder, or clenching of the anus which can exacerbate anal fissure.

In 1993, Khalaf Bushara and David Park were the first to demonstrate a non-muscular use of Botulinum toxin-A. While treating patients with hemifacial spasm, they showed that the botulinum toxin injections inhibit sweating, and so could become useful in treating hyperhidrosis (excessive sweating).  Botulinum toxin-A has since been approved for the treatment of severe primary axillary hyperhidrosis (excessive underarm sweating of unknown cause), which cannot be managed by topical agents.

Botulinum toxin is also currently used to treat disorders of hyperactive nerves besides excessive sweating, such as neuropathic pain, and some allergy symptoms.
In addition to these uses, botulinum toxin is being evaluated for use in treating chronic joint pain.  Studies show that botulinum toxin may be injected into arthritic shoulder joints to reduce chronic pain and improve the joints range of motion.  Another new, albeit odd, cosmetic use for Botulinum toxin is to smooth out the ruddy, wrinkled appearance of a man’s scrotum which is referred to as “Scro-Tox”.

As a physician I need to also address possible adverse effects which are not to be taken lightly.  While botulinum toxin is generally considered safe in a clinical setting, there can be serious side effects from its use.  Most commonly, botulinum toxin can be injected into the wrong muscle group or spread from the intended injection site, causing paralysis of unintended muscles.

These include partial facial paralysis, muscle weakness, and/or trouble swallowing.  Side effects are not limited to direct paralysis however, and can also include headaches, flu-like symptoms, and allergic reactions. Luckily however, just as the cosmetic treatments only last a few months, any adverse effects are also only temporary.  Bruising at the site of injection is not so much a side effect of the toxin but rather from the administration, and is somewhat preventable by the clinician applying pressure to the injection site.  If it does occur, it usually resolves itself within a week to 10 days.

One of the newer forms of botulinum toxin-A is Incobotulinum toxin-A which is branded as Xeomin.  At Optimal Male, although we offer the brand-name Botox, we prefer Xeomin because it has an advantage over other forms. Xeomin contains no binding proteins which keeps the molecules pure and minimizes chances of allergic reactions. Essentially Xeomin is a purer toxin.  Moreover, Xeomin can be kept at room temperature before reconstitution, while Botox needs to be kept either frozen or refrigerated.  An average treatment usually takes about 10-20 minutes.  The physician will inject the Xeomin into the muscles of your forehead, glabella, crows’ feet, armpit, or wherever you and your physician decide treatment may be needed.  No anesthesia is required; however, your physician may use a topical anesthetic or cold pack to reduce any discomfort, which, at most, is minimal.

I would encourage you to visit us for your FREE consultation and exam to further explore how Xeomin may help smooth your wrinkles, reduce joint pain or to stop excessive sweating.  Optimal Male offers some of the most attractive rates in Southwest Florida!

Live Well!

Richard Freier, M.D.
Medical Director
Optimal Male Performance Center
Office: 239.596.8886

*Technical Information on the mechanism of Botulinum

Botulinum works by changing key proteins required for nerve activation.  First, the toxin binds specifically to nerves which use acetylcholine.  After the toxic protein binds to the end of the nerve, it is taken up into a vesicle by receptor-mediated endocytosis.  As the vesicle with the toxin moves farther into the cell, it acidifies, activating a portion of the toxin which triggers it to push across the vesicle membrane and into the cell’s cytoplasm.  Once inside the cytoplasm, the toxin cleaves SNARE proteins (proteins that mediate vesicle fusion, with their target membrane bound compartments) meaning that the acetylcholine vesicles can’t bind to the intracellular cell membrane.  This prevents the cell from releasing vesicles of neurotransmitter.  This stops nerve signaling and leads to paralysis.

Comments are closed.