Bound Newsletter 11.10.2025
At CrossFit Bound, we believe community is more than showing up to train — it’s the energy, trust, and shared effort that lifts everyone higher. A strong community doesn’t just happen; it’s built day by day, through effort, encouragement, and connection. Here’s what makes a community thrive… and what can cause it to stall.
5 Reasons a Community Grows Strong
1. Shared Effort Builds Shared Respect
When people work hard together, barriers break down. Every drop of sweat and every rep builds a level of mutual respect that can’t be faked. It’s not about how much you lift — it’s about showing up and giving your best.
2. Accountability Creates Consistency
Accountability turns intention into action. When your community expects you to show up — and celebrates you when you do — it keeps motivation alive and builds consistency that fuels real, lasting change.
3. Support Through Every Season
A thriving community supports each other not just through workouts, but through life. Injuries, setbacks, and personal challenges happen — and when people rally around each other, that’s when true belonging takes root.
4. Growth Happens Together
When one person improves, everyone benefits. The best communities celebrate each other’s success and use it as inspiration, not comparison. That mindset shifts the culture from competition to collaboration.
5. Purpose Beyond the Whiteboard
The strongest communities know that it’s not just about fitness scores or results. It’s about connection, encouragement, and the belief that we’re all working toward something bigger — together.
5 Reasons a Community Stops Growing
1. Ego Over Effort
When people start focusing on being the best in the room instead of becoming their best selves, community connection breaks down. Ego isolates — effort unites.
2. Lack of Communication
When leaders or members stop communicating — whether it’s about programming, goals, or challenges — small issues turn into big divides. Growth requires openness, honesty, and shared dialogue.
3. Complacency Sets In
Communities stop growing when they stop evolving. When the standard becomes “good enough,” energy fades. Great communities keep raising the bar and finding new ways to challenge and inspire their members.
4. Excluding Instead of Including
When cliques form or new members feel left out, the heartbeat of the community weakens. True strength comes from inclusion — making everyone feel seen, valued, and part of the team.
5. Forgetting the “Why”
When the focus shifts solely to numbers, scores, or profits, the purpose gets lost. Communities grow when they stay grounded in their “why” — the mission to build better humans, not just better athletes.
At CrossFit Bound
We believe community is built one rep, one conversation, and one act of support at a time. Growth doesn’t happen by accident — it happens when people care enough to show up, lift others up, and move forward together.
Final Thoughts
A strong community isn’t defined by its size — it’s defined by its heart. It grows through shared effort, mutual support, and the belief that we’re better together. But it can also fade when ego, silence, or complacency take root. At CrossFit Bound, we choose to keep showing up, to lift each other higher, and to grow together — in fitness, and in life.
Bragging Board
Ryan Boone
Was recently promoted to Lieutenant for Atlanta Fire Department
Abigail Gerleman
Competed in her first Rx Division at the Clash of the Titans this past weekend - reppin the new Bound Shirt!
Attendance for October 2025
1,473 total attendances *clients who checked into a class
Class Averages
5:30am 9.26 avg
5:15pm 9.22 avg
4pm 9.13 avg
12pm 9 avg
9am 7.81 avg
6:30pm 6.39 avg
6:30am 3.25 avg
Committed Club
*16+ classes attended during the month of September
Fernanda Lawler 19
Jen Wells 18
Matthew Kimm 17
Hannah Spratlin 17
Bryan Marichal 16
Katherine Garey 16
Kyle Rice 16
Christopher Kibbe 16
Alyssa Winkler 16
Jeffrey McDonald 16
Jeb Buffington 30
Ryan Boone 28
Sheri Kindred 26
Michael Jamorksi 25
Brittany Karneol 25
Mary Turner 24
Matt Schuster 24
Brian Lawler 24
Elaine Dunbar 23
Natalie Gordon 22
Ruben Rivera 21
Melaine Venable 21
Jullie Chambers 21
Elysia Dunlap 21
Casey Linch 21
Santez Kindred 20
BAM 20
Let’s Welcome New Members
Selvin Paul
Upcoming Anniversaries & Brithdays
Anniversaries
5-years
Fatih Sen - Nov 28
10-years
Rob Morgan - Nov 26
Birthdays
Kristen Humphries - Nov 15
Matt Schuster - Nov 16
Greg Dafini - Nov 18
Julie Chambers - Nov 21
Trevor Wagner - Nov 22
Peter Wiggin - Nov 23
Upcoming Schedule & Events
December 5th - Friday Bound “Lift for a Gift” / Xmas Party
With the holidays requiring so much time and sometimes stress from parties, gatherings, etc. We are going to have a donation to Toys for Tots, workout, and food/party on Friday December 6th at CFB. Bring a Toy to donate, we’ll have a special holiday workout, then enjoy some time and food between 4-7pm.
Wear your favorite Xmas sweater or Grinch Costume and bring a children’s gift.
more details coming soon
Amicolola Falls Marathon - December 6, 2025
Full and Half Marathon route in the famous Amicalola Falls State Park which boasts miles of trails, catering to various fitness levels and preferences. The park's trails meander through lush forests, alongside bubbling creeks, and offer stunning views of the 729-foot Amicalola Falls—the tallest cascading waterfall in Georgia .
Jess and some others are already signed up
The Conquer ‘The Toughest Backyard Ultra’
$150 to sign up, and at the start of the race runners will be given a $100 bill to carry the entire race. The remaining $50 goes to the park fees, volunteers and insurance. If the runner desires to stop or times out of the race, they will place the $100 bill into a glass case for the overall winner to claim at the end. Two years into the planning to discover the toughest location to pull off a backyard ultra and we found it at the famous AT approach trail in the Amicalola Falls State Park. The loop starts at the top of the falls with the rugged East Ridge trail leading down to the bottom parking area to pick up the lower Mountain Laurel trail and then up the AT Approach trails with 605 steps back to the top of the falls.
Simple: Each runner will have 1 hour to complete the 4.1-mile loop (1,065ft of elevation) every hour until only one person remains.
Helen Holiday Half & 10K Race - December 13, 2025
discount code ‘Helen10’. *thank you Jen Wells!
CrossFit Journal Article of the Week: Cholesterol: Villain or Vital?
Rethinking Heart Disease's Public Enemy No. 1
The real story of heart disease risk lies not in your "bad" cholesterol levels, but in markers your doctor probably isn't checking.
By Jocelyn Rylee, MS, CF-L4
In Part 1 of this series, we looked at the history of heart disease and how it rose from a rare and mysterious affliction at the start of the 20th century to the world’s number one killer by the end of it. We looked at competing theories as to its cause, especially sugar vs. saturated fat. Ancel Keys’ “lipid hypothesis” remains prominent today, pointing to saturated fat in the diet raising cholesterol levels in the blood, which causes atherosclerotic plaques to accumulate in the arteries of the heart. But is it true that cholesterol is enemy No. 1 in the battle against heart disease? To explore this question, we must first understand cholesterol itself.
Cholesterol 101
Cholesterol is a waxy, fat-like molecule that is essential to life. It is a type of lipid, but not a fat in the way we typically think of dietary fat. Cholesterol plays a structural role in every cell membrane in the body, helping to regulate fluidity and integrity. Notably, the brain is ~25% cholesterol, and this crucial substance is required to make new brain cells and new neuronal connections. It is also a precursor to several operational systems of the body, including steroid hormones (cortisol, estrogen, and testosterone), vitamin D, and bile acids that help us digest fat. Without cholesterol, our cells would collapse like popped balloons, hormones would vanish, fat would become indigestible, and life as we know it would cease in a biochemical freefall. It’s that important.
Roughly 80% of the cholesterol in your body is made endogenously, primarily by the liver, through a multi-step biochemical pathway (we’ll return to this in the next installment on statins). Only about 20% comes from dietary sources. This internal production is tightly regulated by the body to ensure that adequate cholesterol is available for critical functions. How much cholesterol you consume directly from foods like egg yolks, shrimp, and fish roe has basically no effect on total cholesterol in the blood. If dietary intake of cholesterol decreases, the body compensates by producing more. If intake increases, the body tends to produce less. This built-in feedback loop reflects how essential cholesterol is to survival and cellular function.
The Lipoprotein Carriers
Despite its importance, cholesterol cannot dissolve in water or blood on its own. To travel through the water-based highway of the bloodstream, it must be packaged into specialized transport vehicles called lipoproteins. These lipoproteins are spherical particles made of fats and proteins (hence lipo + protein), which carry cholesterol (along with other cargo like triglycerides and phospholipids) to and from tissues. The most commonly discussed types are low-density lipoprotein (LDL) and high-density lipoprotein (HDL). Less talked about are chylomicrons, Very Low Density Lipoproteins (VLDL), and Intermediate-Density Lipoproteins (IDL). It is essential to distinguish that LDL and HDL are not types of cholesterol; they are carriers of cholesterol. Lipoproteins are like boats or taxis, which may differ in structure and function, but the passengers (cholesterol) are all the same.
The confusion between cholesterol itself and the lipoproteins that carry it has led to widespread misunderstanding. There is no “good cholesterol” and “bad cholesterol.” To be told you have “high cholesterol” — primarily when referring to high TC (aka, Total Cholesterol) — is essentially meaningless. What matters when it comes to predicting future health outcomes is much more nuanced. How many and what types of particles are in circulation? How long have they been in circulation? Have they become oxidized? What health/metabolic states are causing these numbers to be high or low?
Other measurements like LDL particle count (LDL-P), NMR Profile (size and count of particles), Oxidized LDL (oxLDL), and ApoB (apolipoprotein B) offer more meaningful insights. ApoB is a protein found on the surface of each particle (including LDL, VLDL, and IDL), so the total ApoB count reflects the number of particles in circulation.
People with insulin resistance tend to have small, dense LDL particles, which are more likely to penetrate the arterial wall and become oxidized, initiating plaque formation. In contrast, large, buoyant LDL particles are less atherogenic. This is why two people with the same LDL-C can have very different cardiovascular risk profiles.
The Misunderstood Marker
For decades, LDL-C has been the primary focus of cholesterol testing and treatment. But its predictive power is limited. Many people who suffer heart attacks have “normal” LDL-C levels, and many people with elevated LDL-C never experience cardiovascular disease.
One large-scale analysis found that 75% of patients who presented to the hospital for a heart attack had LDL-C levels indicating they were not at high risk for a cardiovascular event, and 50% had levels considered “optimal” (below 100mg/dL or 2.6 mmol/L).
LDL does more than just transport cholesterol. It also plays a vital role in the body’s innate immune system. LDL particles can bind and neutralize bacterial endotoxins such as lipopolysaccharides (LPS), helping to reduce systemic inflammation and infection risk. They act as molecular scavengers, mopping up harmful substances in the bloodstream and delivering them to the liver for disposal. In this way, LDL serves a dual purpose: delivering essential cholesterol to cells while also participating in immune defense, particularly in the early stages of microbial exposure. Low LDL may also leave the immune system weakened and less able to fight early tumor progression in the development of cancer. Research indicates a robust association of low LDL and cancer development, but it is unclear whether low LDL causes cancer or is related in some other way.
Low LDL is consistently shown to be associated with higher mortality, especially in older adults. In simple terms, those with the lowest LDL cholesterol are the most likely to die in the follow-up period (here, here, and here, for example). Perhaps this is because older adults are at higher risk of both cancer and septic infections? Again, the causation (if any) is not clear.
Another wildly interesting observation? Those with low cholesterol levels are also much more likely to commit violent crimes in the future, and low cholesterol is strongly associated with attempted suicide, particularly via violent methods. Since cholesterol is such an integral part of the brain, it is hypothesized that low cholesterol impairs the brain’s ability to engage in executive functions such as mood regulation and impulse control.
The Numbers that Matter
A more nuanced approach to predicting CVD risk considers whether LDL-C levels are discordant with other markers. For example, someone with high LDL-C but low triglycerides and high HDL may be at low risk of CVD, especially if they are metabolically healthy. In the medical literature, this is known as a Lean Mass Hyper-responder phenotype. Conversely, someone with normal LDL-C but high triglycerides and low HDL may be at much greater risk.
One of the most powerful, inexpensive, and underutilized markers for cardiovascular risk is the triglyceride-to-HDL ratio. Research has shown this ratio to be a strong predictor of insulin resistance, metabolic syndrome, and future cardiovascular events. It outperforms LDL-C in predicting risk, particularly in people with normal or borderline LDL levels. The TG:HDL ratio correlates closely with the presence of small, dense LDL particles and other atherogenic changes that accompany poor metabolic health. This simple calculation reflects the state of metabolic health and insulin sensitivity:
A low TG:HDL ratio (<1.5 in mg/dL or <0.87 in mmol/L) suggests good insulin sensitivity.
A high TG:HDL ratio indicates insulin resistance, poor lipid handling, and higher cardiovascular risk.
In short, LDL-C in isolation is a poor marker for heart disease risk and even worse for overall mortality. Looking at the complete metabolic picture provides more accurate and actionable information. Why is there an obsessive focus on lowering LDL-C in the healthcare industry then? Well, unlike LDL-C, there are currently no effective drugs to raise HDL or lower triglycerides in a meaningful way. With nothing to sell to treat those numbers, they get largely ignored. Follow the money, as they say.
In the next article, we’ll explore statins: the most widely prescribed class of cholesterol-lowering drugs. We’ll look at what they actually do, who they help, and what risks they carry.
